---
_id: '9794'
abstract:
- lang: eng
text: 'Lymph nodes (LNs) comprise two main structural elements: fibroblastic reticular
cells that form dedicated niches for immune cell interaction and capsular fibroblasts
that build a shell around the organ. Immunological challenge causes LNs to increase
more than tenfold in size within a few days. Here, we characterized the biomechanics
of LN swelling on the cellular and organ scale. We identified lymphocyte trapping
by influx and proliferation as drivers of an outward pressure force, causing fibroblastic
reticular cells of the T-zone (TRCs) and their associated conduits to stretch.
After an initial phase of relaxation, TRCs sensed the resulting strain through
cell matrix adhesions, which coordinated local growth and remodeling of the stromal
network. While the expanded TRC network readopted its typical configuration, a
massive fibrotic reaction of the organ capsule set in and countered further organ
expansion. Thus, different fibroblast populations mechanically control LN swelling
in a multitier fashion.'
acknowledged_ssus:
- _id: Bio
- _id: EM-Fac
- _id: PreCl
- _id: LifeSc
acknowledgement: This research was supported by the Scientific Service Units of IST
Austria through resources provided by the Imaging and Optics, Electron Microscopy,
Preclinical and Life Science Facilities. We thank C. Moussion for providing anti-PNAd
antibody and D. Critchley for Talin1-floxed mice, and E. Papusheva for providing
a custom 3D channel alignment script. This work was supported by a European Research
Council grant ERC-CoG-72437 to M.S. M.H. was supported by Czech Sciencundation GACR
20-24603Y and Charles University PRIMUS/20/MED/013.
article_processing_charge: No
article_type: original
author:
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Shayan
full_name: Shamipour, Shayan
id: 40B34FE2-F248-11E8-B48F-1D18A9856A87
last_name: Shamipour
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Tommaso
full_name: Costanzo, Tommaso
id: D93824F4-D9BA-11E9-BB12-F207E6697425
last_name: Costanzo
orcid: 0000-0001-9732-3815
- first_name: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Burkhard
full_name: Ludewig, Burkhard
last_name: Ludewig
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Wolfgang
full_name: Weninger, Wolfgang
last_name: Weninger
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Sanjiv A.
full_name: Luther, Sanjiv A.
last_name: Luther
- first_name: Jens V.
full_name: Stein, Jens V.
last_name: Stein
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-4561-241X
citation:
ama: Assen FP, Abe J, Hons M, et al. Multitier mechanics control stromal adaptations
in swelling lymph nodes. Nature Immunology. 2022;23:1246-1255. doi:10.1038/s41590-022-01257-4
apa: Assen, F. P., Abe, J., Hons, M., Hauschild, R., Shamipour, S., Kaufmann, W.,
… Sixt, M. K. (2022). Multitier mechanics control stromal adaptations in swelling
lymph nodes. Nature Immunology. Springer Nature. https://doi.org/10.1038/s41590-022-01257-4
chicago: Assen, Frank P, Jun Abe, Miroslav Hons, Robert Hauschild, Shayan Shamipour,
Walter Kaufmann, Tommaso Costanzo, et al. “Multitier Mechanics Control Stromal
Adaptations in Swelling Lymph Nodes.” Nature Immunology. Springer Nature,
2022. https://doi.org/10.1038/s41590-022-01257-4.
ieee: F. P. Assen et al., “Multitier mechanics control stromal adaptations
in swelling lymph nodes,” Nature Immunology, vol. 23. Springer Nature,
pp. 1246–1255, 2022.
ista: Assen FP, Abe J, Hons M, Hauschild R, Shamipour S, Kaufmann W, Costanzo T,
Krens G, Brown M, Ludewig B, Hippenmeyer S, Heisenberg C-PJ, Weninger W, Hannezo
EB, Luther SA, Stein JV, Sixt MK. 2022. Multitier mechanics control stromal adaptations
in swelling lymph nodes. Nature Immunology. 23, 1246–1255.
mla: Assen, Frank P., et al. “Multitier Mechanics Control Stromal Adaptations in
Swelling Lymph Nodes.” Nature Immunology, vol. 23, Springer Nature, 2022,
pp. 1246–55, doi:10.1038/s41590-022-01257-4.
short: F.P. Assen, J. Abe, M. Hons, R. Hauschild, S. Shamipour, W. Kaufmann, T.
Costanzo, G. Krens, M. Brown, B. Ludewig, S. Hippenmeyer, C.-P.J. Heisenberg,
W. Weninger, E.B. Hannezo, S.A. Luther, J.V. Stein, M.K. Sixt, Nature Immunology
23 (2022) 1246–1255.
date_created: 2021-08-06T09:09:11Z
date_published: 2022-07-11T00:00:00Z
date_updated: 2023-08-02T06:53:07Z
day: '11'
ddc:
- '570'
department:
- _id: SiHi
- _id: CaHe
- _id: EdHa
- _id: EM-Fac
- _id: Bio
- _id: MiSi
doi: 10.1038/s41590-022-01257-4
ec_funded: 1
external_id:
isi:
- '000822975900002'
file:
- access_level: open_access
checksum: 628e7b49809f22c75b428842efe70c68
content_type: application/pdf
creator: dernst
date_created: 2022-07-25T07:11:32Z
date_updated: 2022-07-25T07:11:32Z
file_id: '11642'
file_name: 2022_NatureImmunology_Assen.pdf
file_size: 11475325
relation: main_file
success: 1
file_date_updated: 2022-07-25T07:11:32Z
has_accepted_license: '1'
intvolume: ' 23'
isi: 1
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: 1246-1255
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
publication: Nature Immunology
publication_identifier:
eissn:
- 1529-2916
issn:
- 1529-2908
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Multitier mechanics control stromal adaptations in swelling lymph nodes
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 23
year: '2022'
...
---
_id: '275'
abstract:
- lang: eng
text: Lymphatic endothelial cells (LECs) release extracellular chemokines to guide
the migration of dendritic cells. In this study, we report that LECs also release
basolateral exosome-rich endothelial vesicles (EEVs) that are secreted in greater
numbers in the presence of inflammatory cytokines and accumulate in the perivascular
stroma of small lymphatic vessels in human chronic inflammatory diseases. Proteomic
analyses of EEV fractions identified > 1,700 cargo proteins and revealed a
dominant motility-promoting protein signature. In vitro and ex vivo EEV fractions
augmented cellular protrusion formation in a CX3CL1/fractalkine-dependent fashion
and enhanced the directional migratory response of human dendritic cells along
guidance cues. We conclude that perilymphatic LEC exosomes enhance exploratory
behavior and thus promote directional migration of CX3CR1-expressing cells in
complex tissue environments.
acknowledgement: M. Brown was supported by the Cell Communication in Health and Disease
Graduate Study Program of the Austrian Science Fund and Medizinische Universität
Wien, M. Sixt by the European Research Council (ERC GA 281556) and an Austrian Science
Fund START award, K.L. Bennett by the Austrian Academy of Sciences, D.G. Jackson
and L.A. Johnson by Unit Funding (MC_UU_12010/2) and project grants from the Medical
Research Council (G1100134 and MR/L008610/1), and M. Detmar by the Schweizerischer
Nationalfonds zur Förderung der Wissenschaftlichen Forschung and Advanced European
Research Council grant LYVICAM. K. Vaahtomeri was supported by an Academy of Finland
postdoctoral research grant (287853). This project has received funding from the
European Union’s Horizon 2020 research and innovation program under grant agreement
No. 668036 (RELENT).
article_processing_charge: No
author:
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Louise
full_name: Johnson, Louise
last_name: Johnson
- first_name: Dario
full_name: Leone, Dario
last_name: Leone
- first_name: Peter
full_name: Májek, Peter
last_name: Májek
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Daniel
full_name: Senfter, Daniel
last_name: Senfter
- first_name: Nora
full_name: Bukosza, Nora
last_name: Bukosza
- first_name: Helga
full_name: Schachner, Helga
last_name: Schachner
- first_name: Gabriele
full_name: Asfour, Gabriele
last_name: Asfour
- first_name: Brigitte
full_name: Langer, Brigitte
last_name: Langer
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Katja
full_name: Parapatics, Katja
last_name: Parapatics
- first_name: Young
full_name: Hong, Young
last_name: Hong
- first_name: Keiryn
full_name: Bennett, Keiryn
last_name: Bennett
- first_name: Renate
full_name: Kain, Renate
last_name: Kain
- first_name: Michael
full_name: Detmar, Michael
last_name: Detmar
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: David
full_name: Jackson, David
last_name: Jackson
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
citation:
ama: Brown M, Johnson L, Leone D, et al. Lymphatic exosomes promote dendritic cell
migration along guidance cues. Journal of Cell Biology. 2018;217(6):2205-2221.
doi:10.1083/jcb.201612051
apa: Brown, M., Johnson, L., Leone, D., Májek, P., Vaahtomeri, K., Senfter, D.,
… Kerjaschki, D. (2018). Lymphatic exosomes promote dendritic cell migration along
guidance cues. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201612051
chicago: Brown, Markus, Louise Johnson, Dario Leone, Peter Májek, Kari Vaahtomeri,
Daniel Senfter, Nora Bukosza, et al. “Lymphatic Exosomes Promote Dendritic Cell
Migration along Guidance Cues.” Journal of Cell Biology. Rockefeller University
Press, 2018. https://doi.org/10.1083/jcb.201612051.
ieee: M. Brown et al., “Lymphatic exosomes promote dendritic cell migration
along guidance cues,” Journal of Cell Biology, vol. 217, no. 6. Rockefeller
University Press, pp. 2205–2221, 2018.
ista: Brown M, Johnson L, Leone D, Májek P, Vaahtomeri K, Senfter D, Bukosza N,
Schachner H, Asfour G, Langer B, Hauschild R, Parapatics K, Hong Y, Bennett K,
Kain R, Detmar M, Sixt MK, Jackson D, Kerjaschki D. 2018. Lymphatic exosomes promote
dendritic cell migration along guidance cues. Journal of Cell Biology. 217(6),
2205–2221.
mla: Brown, Markus, et al. “Lymphatic Exosomes Promote Dendritic Cell Migration
along Guidance Cues.” Journal of Cell Biology, vol. 217, no. 6, Rockefeller
University Press, 2018, pp. 2205–21, doi:10.1083/jcb.201612051.
short: M. Brown, L. Johnson, D. Leone, P. Májek, K. Vaahtomeri, D. Senfter, N. Bukosza,
H. Schachner, G. Asfour, B. Langer, R. Hauschild, K. Parapatics, Y. Hong, K. Bennett,
R. Kain, M. Detmar, M.K. Sixt, D. Jackson, D. Kerjaschki, Journal of Cell Biology
217 (2018) 2205–2221.
date_created: 2018-12-11T11:45:33Z
date_published: 2018-04-12T00:00:00Z
date_updated: 2023-09-13T08:51:29Z
day: '12'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
doi: 10.1083/jcb.201612051
ec_funded: 1
external_id:
isi:
- '000438077800026'
pmid:
- '29650776'
file:
- access_level: open_access
checksum: 9c7eba51a35c62da8c13f98120b64df4
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T12:50:07Z
date_updated: 2020-07-14T12:45:45Z
file_id: '5704'
file_name: 2018_JournalCellBiology_Brown.pdf
file_size: 2252043
relation: main_file
file_date_updated: 2020-07-14T12:45:45Z
has_accepted_license: '1'
intvolume: ' 217'
isi: 1
issue: '6'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 2205 - 2221
pmid: 1
project:
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Journal of Cell Biology
publication_status: published
publisher: Rockefeller University Press
publist_id: '7627'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Lymphatic exosomes promote dendritic cell migration along guidance cues
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 217
year: '2018'
...
---
_id: '402'
abstract:
- lang: eng
text: During metastasis, malignant cells escape the primary tumor, intravasate lymphatic
vessels, and reach draining sentinel lymph nodes before they colonize distant
organs via the blood circulation. Although lymph node metastasis in cancer patients
correlates with poor prognosis, evidence is lacking as to whether and how tumor
cells enter the bloodstream via lymph nodes. To investigate this question, we
delivered carcinoma cells into the lymph nodes of mice by microinfusing the cells
into afferent lymphatic vessels. We found that tumor cells rapidly infiltrated
the lymph node parenchyma, invaded blood vessels, and seeded lung metastases without
involvement of the thoracic duct. These results suggest that the lymph node blood
vessels can serve as an exit route for systemic dissemination of cancer cells
in experimental mouse models. Whether this form of tumor cell spreading occurs
in cancer patients remains to be determined.
acknowledged_ssus:
- _id: Bio
acknowledgement: "M.B. was supported by the Cell Communication in Health and Disease
graduate study program of the Austrian Science Fund (FWF) and the Medical University
of Vienna. M.S. was supported by the European Research Council (grant ERC GA 281556)
and an FWF START award.\r\nWe thank C. Moussion for establishing the intralymphatic
injection at IST Austria and for providing anti-PNAd hybridoma supernatant, R. Förster
and A. Braun for sharing the intralymphatic injection technology, K. Vaahtomeri
for the lentiviral constructs, M. Hons for establishing in vivo multiphoton imaging,
the Sixt lab for intellectual input, M. Schunn for help with the design of the in
vivo experiments, F. Langer for technical assistance with the in vivo experiments,
the bioimaging facility of IST Austria for support, and R. Efferl for providing
the CT26 cell line."
article_processing_charge: No
article_type: original
author:
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Helga
full_name: Schachner, Helga
last_name: Schachner
- first_name: Gabriele
full_name: Asfour, Gabriele
last_name: Asfour
- first_name: Zsuzsanna
full_name: Bagó Horváth, Zsuzsanna
last_name: Bagó Horváth
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: Pavel
full_name: Uhrin, Pavel
last_name: Uhrin
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
citation:
ama: Brown M, Assen FP, Leithner AF, et al. Lymph node blood vessels provide exit
routes for metastatic tumor cell dissemination in mice. Science. 2018;359(6382):1408-1411.
doi:10.1126/science.aal3662
apa: Brown, M., Assen, F. P., Leithner, A. F., Abe, J., Schachner, H., Asfour, G.,
… Kerjaschki, D. (2018). Lymph node blood vessels provide exit routes for metastatic
tumor cell dissemination in mice. Science. American Association for the
Advancement of Science. https://doi.org/10.1126/science.aal3662
chicago: Brown, Markus, Frank P Assen, Alexander F Leithner, Jun Abe, Helga Schachner,
Gabriele Asfour, Zsuzsanna Bagó Horváth, et al. “Lymph Node Blood Vessels Provide
Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science.
American Association for the Advancement of Science, 2018. https://doi.org/10.1126/science.aal3662.
ieee: M. Brown et al., “Lymph node blood vessels provide exit routes for
metastatic tumor cell dissemination in mice,” Science, vol. 359, no. 6382.
American Association for the Advancement of Science, pp. 1408–1411, 2018.
ista: Brown M, Assen FP, Leithner AF, Abe J, Schachner H, Asfour G, Bagó Horváth
Z, Stein J, Uhrin P, Sixt MK, Kerjaschki D. 2018. Lymph node blood vessels provide
exit routes for metastatic tumor cell dissemination in mice. Science. 359(6382),
1408–1411.
mla: Brown, Markus, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic
Tumor Cell Dissemination in Mice.” Science, vol. 359, no. 6382, American
Association for the Advancement of Science, 2018, pp. 1408–11, doi:10.1126/science.aal3662.
short: M. Brown, F.P. Assen, A.F. Leithner, J. Abe, H. Schachner, G. Asfour, Z.
Bagó Horváth, J. Stein, P. Uhrin, M.K. Sixt, D. Kerjaschki, Science 359 (2018)
1408–1411.
date_created: 2018-12-11T11:46:16Z
date_published: 2018-03-23T00:00:00Z
date_updated: 2024-03-25T23:30:05Z
day: '23'
department:
- _id: MiSi
doi: 10.1126/science.aal3662
ec_funded: 1
external_id:
isi:
- '000428043600047'
pmid:
- '29567714'
intvolume: ' 359'
isi: 1
issue: '6382'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1126/science.aal3662
month: '03'
oa: 1
oa_version: Published Version
page: 1408 - 1411
pmid: 1
project:
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7428'
quality_controlled: '1'
related_material:
record:
- id: '6947'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination
in mice
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 359
year: '2018'
...
---
_id: '672'
abstract:
- lang: eng
text: Trafficking cells frequently transmigrate through epithelial and endothelial
monolayers. How monolayers cooperate with the penetrating cells to support their
transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic
capillaries as a model system for transendothelial migration. We find that the
chemokine CCL21, which is the decisive guidance cue for intravasation, mainly
localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial
cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes
extracellularly enriched at the sites of endothelial cell-cell junctions. When
we reconstitute the transmigration process in vitro, we find that secretion of
CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and
selective calcium chelation in lymphatic endothelium attenuates transmigration.
Altogether, our data demonstrate a chemokine-mediated feedback between DCs and
lymphatic endothelium, which facilitates transendothelial migration.
article_processing_charge: Yes
author:
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
- first_name: Matthias
full_name: Mehling, Matthias
id: 3C23B994-F248-11E8-B48F-1D18A9856A87
last_name: Mehling
orcid: 0000-0001-8599-1226
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the
chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia.
Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027
apa: Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling,
M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes
dendritic cell transmigration across lymphatic endothelia. Cell Reports.
Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027
chicago: Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander
F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered
Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic
Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027.
ieee: K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21
promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports,
vol. 19, no. 5. Cell Press, pp. 902–909, 2017.
ista: Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann
W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic
cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.
mla: Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21
Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports,
vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027.
short: K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling,
W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.
date_created: 2018-12-11T11:47:50Z
date_published: 2017-05-02T00:00:00Z
date_updated: 2023-02-23T12:50:09Z
day: '02'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
- _id: EM-Fac
doi: 10.1016/j.celrep.2017.04.027
ec_funded: 1
file:
- access_level: open_access
checksum: 8fdddaab1f1d76a6ec9ca94dcb6b07a2
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:54Z
date_updated: 2020-07-14T12:47:38Z
file_id: '5109'
file_name: IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf
file_size: 2248814
relation: main_file
file_date_updated: 2020-07-14T12:47:38Z
has_accepted_license: '1'
intvolume: ' 19'
issue: '5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 902 - 909
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Cell Reports
publication_identifier:
issn:
- '22111247'
publication_status: published
publisher: Cell Press
publist_id: '7052'
pubrep_id: '900'
quality_controlled: '1'
scopus_import: 1
status: public
title: Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration
across lymphatic endothelia
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '674'
abstract:
- lang: eng
text: Navigation of cells along gradients of guidance cues is a determining step
in many developmental and immunological processes. Gradients can either be soluble
or immobilized to tissues as demonstrated for the haptotactic migration of dendritic
cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate
how gradient characteristics govern cellular response patterns, we here introduce
an in vitro system allowing to track migratory responses of DCs to precisely controlled
immobilized gradients of CCL21. We find that haptotactic sensing depends on the
absolute CCL21 concentration and local steepness of the gradient, consistent with
a scenario where DC directionality is governed by the signal-to-noise ratio of
CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC
guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore,
we find that CCR7 signal termination by the G-protein-coupled receptor kinase
6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient
sensing in vitro and confirm those observations in vivo. These findings suggest
that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal
guidance in vivo.
author:
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Veronika
full_name: Bierbaum, Veronika
id: 3FD04378-F248-11E8-B48F-1D18A9856A87
last_name: Bierbaum
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Teresa
full_name: Tarrant, Teresa
last_name: Tarrant
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic
chemokine gradients in a manner governed by signal to noise ratio and dependent
on GRK6. Current Biology. 2017;27(9):1314-1325. doi:10.1016/j.cub.2017.04.004
apa: Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries,
I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients
in a manner governed by signal to noise ratio and dependent on GRK6. Current
Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.04.004
chicago: Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus
Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret
Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio
and Dependent on GRK6.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.04.004.
ieee: J. Schwarz et al., “Dendritic cells interpret haptotactic chemokine
gradients in a manner governed by signal to noise ratio and dependent on GRK6,”
Current Biology, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017.
ista: Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner
AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells
interpret haptotactic chemokine gradients in a manner governed by signal to noise
ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325.
mla: Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients
in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current
Biology, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:10.1016/j.cub.2017.04.004.
short: J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries,
A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt,
Current Biology 27 (2017) 1314–1325.
date_created: 2018-12-11T11:47:51Z
date_published: 2017-05-09T00:00:00Z
date_updated: 2023-02-23T12:50:44Z
day: '09'
department:
- _id: MiSi
- _id: Bio
- _id: NanoFab
doi: 10.1016/j.cub.2017.04.004
ec_funded: 1
intvolume: ' 27'
issue: '9'
language:
- iso: eng
month: '05'
oa_version: None
page: 1314 - 1325
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Current Biology
publication_identifier:
issn:
- '09609822'
publication_status: published
publisher: Cell Press
publist_id: '7050'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dendritic cells interpret haptotactic chemokine gradients in a manner governed
by signal to noise ratio and dependent on GRK6
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 27
year: '2017'
...
---
_id: '1142'
abstract:
- lang: eng
text: Hemolysis drives susceptibility to bacterial infections and predicts poor
outcome from sepsis. These detrimental effects are commonly considered to be a
consequence of heme-iron serving as a nutrient for bacteria. We employed a Gram-negative
sepsis model and found that elevated heme levels impaired the control of bacterial
proliferation independently of heme-iron acquisition by pathogens. Heme strongly
inhibited phagocytosis and the migration of human and mouse phagocytes by disrupting
actin cytoskeletal dynamics via activation of the GTP-binding Rho family protein
Cdc42 by the guanine nucleotide exchange factor DOCK8. A chemical screening approach
revealed that quinine effectively prevented heme effects on the cytoskeleton,
restored phagocytosis and improved survival in sepsis. These mechanistic insights
provide potential therapeutic targets for patients with sepsis or hemolytic disorders.
acknowledgement: 'Y. Fukui (Medical Institute of Bioregulation, Kyushu University)
and J. Stein (Theodor Kocher Institute, University of Bern) are acknowledged for
providing the DOCK8 deficient bone marrow. and H. Häcker (St. Judes Children''s
Research Hospital) for providing the ERHBD-HoxB8-encoding retroviral construct.
pSpCas9(BB)-2a-Puro (PX459) was a gift from F. Zhang (Massachusetts Institute of
Technology) (Addgene plasmid # 48139) and pGRG36 was a gift from N. Craig (Johns
Hopkins University School of Medicine) (Addgene plasmid # 16666). LifeAct-GFP-encoding
retrovirus was kindly provided by A. Leithner (Institute of Science and Technology
Austria). pSIM8 and TKC E. coli were gifts from D.L. Court (Center for Cancer Research,
National Cancer Institute). We acknowledge M. Gröger and S. Rauscher for excellent
technical support (Core imaging facility, Medical University of Vienna). We thank
D.P. Barlow and L.R. Cheever for critical reading of the manuscript. This work was
supported by the Austrian Academy of Sciences, the Science Fund of the Austrian
National Bank (14107) and the Austrian Science Fund FWF (I1620-B22) in the Infect-ERA
framework (to S.Knapp).'
author:
- first_name: Rui
full_name: Martins, Rui
last_name: Martins
- first_name: Julia
full_name: Maier, Julia
last_name: Maier
- first_name: Anna
full_name: Gorki, Anna
last_name: Gorki
- first_name: Kilian
full_name: Huber, Kilian
last_name: Huber
- first_name: Omar
full_name: Sharif, Omar
last_name: Sharif
- first_name: Philipp
full_name: Starkl, Philipp
last_name: Starkl
- first_name: Simona
full_name: Saluzzo, Simona
last_name: Saluzzo
- first_name: Federica
full_name: Quattrone, Federica
last_name: Quattrone
- first_name: Riem
full_name: Gawish, Riem
last_name: Gawish
- first_name: Karin
full_name: Lakovits, Karin
last_name: Lakovits
- first_name: Michael
full_name: Aichinger, Michael
last_name: Aichinger
- first_name: Branka
full_name: Radic Sarikas, Branka
last_name: Radic Sarikas
- first_name: Charles
full_name: Lardeau, Charles
last_name: Lardeau
- first_name: Anastasiya
full_name: Hladik, Anastasiya
last_name: Hladik
- first_name: Ana
full_name: Korosec, Ana
last_name: Korosec
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Michelle
full_name: Duggan, Michelle
id: 2EDEA62C-F248-11E8-B48F-1D18A9856A87
last_name: Duggan
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
- first_name: Harald
full_name: Esterbauer, Harald
last_name: Esterbauer
- first_name: Jacques
full_name: Colinge, Jacques
last_name: Colinge
- first_name: Stephanie
full_name: Eisenbarth, Stephanie
last_name: Eisenbarth
- first_name: Thomas
full_name: Decker, Thomas
last_name: Decker
- first_name: Keiryn
full_name: Bennett, Keiryn
last_name: Bennett
- first_name: Stefan
full_name: Kubicek, Stefan
last_name: Kubicek
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Giulio
full_name: Superti Furga, Giulio
last_name: Superti Furga
- first_name: Sylvia
full_name: Knapp, Sylvia
last_name: Knapp
citation:
ama: Martins R, Maier J, Gorki A, et al. Heme drives hemolysis-induced susceptibility
to infection via disruption of phagocyte functions. Nature Immunology.
2016;17(12):1361-1372. doi:10.1038/ni.3590
apa: Martins, R., Maier, J., Gorki, A., Huber, K., Sharif, O., Starkl, P., … Knapp,
S. (2016). Heme drives hemolysis-induced susceptibility to infection via disruption
of phagocyte functions. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3590
chicago: Martins, Rui, Julia Maier, Anna Gorki, Kilian Huber, Omar Sharif, Philipp
Starkl, Simona Saluzzo, et al. “Heme Drives Hemolysis-Induced Susceptibility to
Infection via Disruption of Phagocyte Functions.” Nature Immunology. Nature
Publishing Group, 2016. https://doi.org/10.1038/ni.3590.
ieee: R. Martins et al., “Heme drives hemolysis-induced susceptibility to
infection via disruption of phagocyte functions,” Nature Immunology, vol.
17, no. 12. Nature Publishing Group, pp. 1361–1372, 2016.
ista: Martins R, Maier J, Gorki A, Huber K, Sharif O, Starkl P, Saluzzo S, Quattrone
F, Gawish R, Lakovits K, Aichinger M, Radic Sarikas B, Lardeau C, Hladik A, Korosec
A, Brown M, Vaahtomeri K, Duggan M, Kerjaschki D, Esterbauer H, Colinge J, Eisenbarth
S, Decker T, Bennett K, Kubicek S, Sixt MK, Superti Furga G, Knapp S. 2016. Heme
drives hemolysis-induced susceptibility to infection via disruption of phagocyte
functions. Nature Immunology. 17(12), 1361–1372.
mla: Martins, Rui, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection
via Disruption of Phagocyte Functions.” Nature Immunology, vol. 17, no.
12, Nature Publishing Group, 2016, pp. 1361–72, doi:10.1038/ni.3590.
short: R. Martins, J. Maier, A. Gorki, K. Huber, O. Sharif, P. Starkl, S. Saluzzo,
F. Quattrone, R. Gawish, K. Lakovits, M. Aichinger, B. Radic Sarikas, C. Lardeau,
A. Hladik, A. Korosec, M. Brown, K. Vaahtomeri, M. Duggan, D. Kerjaschki, H. Esterbauer,
J. Colinge, S. Eisenbarth, T. Decker, K. Bennett, S. Kubicek, M.K. Sixt, G. Superti
Furga, S. Knapp, Nature Immunology 17 (2016) 1361–1372.
date_created: 2018-12-11T11:50:22Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2021-01-12T06:48:36Z
day: '01'
department:
- _id: MiSi
- _id: PeJo
doi: 10.1038/ni.3590
intvolume: ' 17'
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d
month: '12'
oa: 1
oa_version: Submitted Version
page: 1361 - 1372
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '6216'
quality_controlled: '1'
scopus_import: 1
status: public
title: Heme drives hemolysis-induced susceptibility to infection via disruption of
phagocyte functions
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 17
year: '2016'
...
---
_id: '1321'
abstract:
- lang: eng
text: Most migrating cells extrude their front by the force of actin polymerization.
Polymerization requires an initial nucleation step, which is mediated by factors
establishing either parallel filaments in the case of filopodia or branched filaments
that form the branched lamellipodial network. Branches are considered essential
for regular cell motility and are initiated by the Arp2/3 complex, which in turn
is activated by nucleation-promoting factors of the WASP and WAVE families. Here
we employed rapid amoeboid crawling leukocytes and found that deletion of the
WAVE complex eliminated actin branching and thus lamellipodia formation. The cells
were left with parallel filaments at the leading edge, which translated, depending
on the differentiation status of the cell, into a unipolar pointed cell shape
or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased
speed and enormous directional persistence, while they were unable to turn towards
chemotactic gradients. Cells with multiple filopodia retained chemotactic activity
but their migration was progressively impaired with increasing geometrical complexity
of the extracellular environment. These findings establish that diversified leading
edge protrusions serve as explorative structures while they slow down actual locomotion.
acknowledged_ssus:
- _id: SSU
acknowledgement: "This work was supported by the German Research Foundation (DFG)
Priority Program SP 1464 to T.E.B.S. and M.S., and European Research Council (ERC
GA 281556) and Human Frontiers Program grants to M.S.\r\nService Units of IST Austria
for excellent technical support."
article_processing_charge: No
article_type: original
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: David
full_name: De Gorter, David
last_name: De Gorter
- first_name: Florian
full_name: Schur, Florian
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
- first_name: Jonathan
full_name: Bayerl, Jonathan
last_name: Bayerl
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Stefan
full_name: Wieser, Stefan
id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
last_name: Wieser
orcid: 0000-0002-2670-2217
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Frank
full_name: Lai, Frank
last_name: Lai
- first_name: Markus
full_name: Moser, Markus
last_name: Moser
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Victor
full_name: Small, Victor
last_name: Small
- first_name: Theresia
full_name: Stradal, Theresia
last_name: Stradal
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Leithner AF, Eichner A, Müller J, et al. Diversified actin protrusions promote
environmental exploration but are dispensable for locomotion of leukocytes. Nature
Cell Biology. 2016;18:1253-1259. doi:10.1038/ncb3426
apa: Leithner, A. F., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz,
J., … Sixt, M. K. (2016). Diversified actin protrusions promote environmental
exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology.
Nature Publishing Group. https://doi.org/10.1038/ncb3426
chicago: Leithner, Alexander F, Alexander Eichner, Jan Müller, Anne Reversat, Markus
Brown, Jan Schwarz, Jack Merrin, et al. “Diversified Actin Protrusions Promote
Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature
Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/ncb3426.
ieee: A. F. Leithner et al., “Diversified actin protrusions promote environmental
exploration but are dispensable for locomotion of leukocytes,” Nature Cell
Biology, vol. 18. Nature Publishing Group, pp. 1253–1259, 2016.
ista: Leithner AF, Eichner A, Müller J, Reversat A, Brown M, Schwarz J, Merrin J,
De Gorter D, Schur FK, Bayerl J, de Vries I, Wieser S, Hauschild R, Lai F, Moser
M, Kerjaschki D, Rottner K, Small V, Stradal T, Sixt MK. 2016. Diversified actin
protrusions promote environmental exploration but are dispensable for locomotion
of leukocytes. Nature Cell Biology. 18, 1253–1259.
mla: Leithner, Alexander F., et al. “Diversified Actin Protrusions Promote Environmental
Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell
Biology, vol. 18, Nature Publishing Group, 2016, pp. 1253–59, doi:10.1038/ncb3426.
short: A.F. Leithner, A. Eichner, J. Müller, A. Reversat, M. Brown, J. Schwarz,
J. Merrin, D. De Gorter, F.K. Schur, J. Bayerl, I. de Vries, S. Wieser, R. Hauschild,
F. Lai, M. Moser, D. Kerjaschki, K. Rottner, V. Small, T. Stradal, M.K. Sixt,
Nature Cell Biology 18 (2016) 1253–1259.
date_created: 2018-12-11T11:51:21Z
date_published: 2016-10-24T00:00:00Z
date_updated: 2024-03-25T23:30:09Z
day: '24'
ddc:
- '570'
department:
- _id: MiSi
- _id: NanoFab
- _id: Bio
doi: 10.1038/ncb3426
ec_funded: 1
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checksum: e1411cb7c99a2d9089c178a6abef25e7
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creator: dernst
date_created: 2020-05-14T16:33:46Z
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file_name: 2018_NatureCell_Leithner.pdf
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language:
- iso: eng
month: '10'
oa: 1
oa_version: Submitted Version
page: 1253 - 1259
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '5949'
quality_controlled: '1'
related_material:
record:
- id: '323'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Diversified actin protrusions promote environmental exploration but are dispensable
for locomotion of leukocytes
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 18
year: '2016'
...
---
_id: '2283'
abstract:
- lang: eng
text: Pathogens exert a strong selection pressure on organisms to evolve effective
immune defences. In addition to individual immunity, social organisms can act
cooperatively to produce collective defences. In many ant species, queens have
the option to found a colony alone or in groups with other, often unrelated, conspecifics.
These associations are transient, usually lasting only as long as each queen benefits
from the presence of others. In fact, once the first workers emerge, queens fight
to the death for dominance. One potential advantage of co-founding may be that
queens benefit from collective disease defences, such as mutual grooming, that
act against common soil pathogens. We test this hypothesis by exposing single
and co-founding queens to a fungal parasite, in order to assess whether queens
in co-founding associations have improved survival. Surprisingly, co-foundresses
exposed to the entomopathogenic fungus Metarhizium did not engage in cooperative
disease defences, and consequently, we find no direct benefit of multiple queens
on survival. However, an indirect benefit was observed, with parasite-exposed
queens producing more brood when they co-founded, than when they were alone. We
suggest this is due to a trade-off between reproduction and immunity. Additionally,
we report an extraordinary ability of the queens to tolerate an infection for
long periods after parasite exposure. Our study suggests that there are no social
immunity benefits for co-founding ant queens, but that in parasite-rich environments,
the presence of additional queens may nevertheless improve the chances of colony
founding success.
author:
- first_name: Christopher
full_name: Pull, Christopher
id: 3C7F4840-F248-11E8-B48F-1D18A9856A87
last_name: Pull
orcid: 0000-0003-1122-3982
- first_name: William
full_name: Hughes, William
last_name: Hughes
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
citation:
ama: 'Pull C, Hughes W, Brown M. Tolerating an infection: an indirect benefit of
co-founding queen associations in the ant Lasius niger . Naturwissenschaften.
2013;100(12):1125-1136. doi:10.1007/s00114-013-1115-5'
apa: 'Pull, C., Hughes, W., & Brown, M. (2013). Tolerating an infection: an
indirect benefit of co-founding queen associations in the ant Lasius niger . Naturwissenschaften.
Springer. https://doi.org/10.1007/s00114-013-1115-5'
chicago: 'Pull, Christopher, William Hughes, and Markus Brown. “Tolerating an Infection:
An Indirect Benefit of Co-Founding Queen Associations in the Ant Lasius Niger
.” Naturwissenschaften. Springer, 2013. https://doi.org/10.1007/s00114-013-1115-5.'
ieee: 'C. Pull, W. Hughes, and M. Brown, “Tolerating an infection: an indirect benefit
of co-founding queen associations in the ant Lasius niger ,” Naturwissenschaften,
vol. 100, no. 12. Springer, pp. 1125–1136, 2013.'
ista: 'Pull C, Hughes W, Brown M. 2013. Tolerating an infection: an indirect benefit
of co-founding queen associations in the ant Lasius niger . Naturwissenschaften.
100(12), 1125–1136.'
mla: 'Pull, Christopher, et al. “Tolerating an Infection: An Indirect Benefit of
Co-Founding Queen Associations in the Ant Lasius Niger .” Naturwissenschaften,
vol. 100, no. 12, Springer, 2013, pp. 1125–36, doi:10.1007/s00114-013-1115-5.'
short: C. Pull, W. Hughes, M. Brown, Naturwissenschaften 100 (2013) 1125–1136.
date_created: 2018-12-11T11:56:45Z
date_published: 2013-11-14T00:00:00Z
date_updated: 2021-01-12T06:56:31Z
day: '14'
department:
- _id: SyCr
doi: 10.1007/s00114-013-1115-5
intvolume: ' 100'
issue: '12'
language:
- iso: eng
month: '11'
oa_version: None
page: 1125 - 1136
publication: Naturwissenschaften
publication_status: published
publisher: Springer
publist_id: '4649'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Tolerating an infection: an indirect benefit of co-founding queen associations
in the ant Lasius niger '
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 100
year: '2013'
...