[{"acknowledged_ssus":[{"_id":"Bio"},{"_id":"EM-Fac"},{"_id":"PreCl"},{"_id":"LifeSc"}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","short":"CC BY (4.0)"},"intvolume":"        23","abstract":[{"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.","lang":"eng"}],"has_accepted_license":"1","file_date_updated":"2022-07-25T07:11:32Z","publication_status":"published","publication_identifier":{"eissn":["1529-2916"],"issn":["1529-2908"]},"title":"Multitier mechanics control stromal adaptations in swelling lymph nodes","oa_version":"Published Version","day":"11","scopus_import":"1","author":[{"last_name":"Assen","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","full_name":"Assen, Frank P","orcid":"0000-0003-3470-6119","first_name":"Frank P"},{"last_name":"Abe","full_name":"Abe, Jun","first_name":"Jun"},{"last_name":"Hons","id":"4167FE56-F248-11E8-B48F-1D18A9856A87","full_name":"Hons, Miroslav","first_name":"Miroslav","orcid":"0000-0002-6625-3348"},{"orcid":"0000-0001-9843-3522","first_name":"Robert","last_name":"Hauschild","full_name":"Hauschild, Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Shamipour, Shayan","id":"40B34FE2-F248-11E8-B48F-1D18A9856A87","last_name":"Shamipour","first_name":"Shayan"},{"first_name":"Walter","orcid":"0000-0001-9735-5315","last_name":"Kaufmann","id":"3F99E422-F248-11E8-B48F-1D18A9856A87","full_name":"Kaufmann, Walter"},{"orcid":"0000-0001-9732-3815","first_name":"Tommaso","id":"D93824F4-D9BA-11E9-BB12-F207E6697425","full_name":"Costanzo, Tommaso","last_name":"Costanzo"},{"full_name":"Krens, Gabriel","id":"2B819732-F248-11E8-B48F-1D18A9856A87","last_name":"Krens","first_name":"Gabriel","orcid":"0000-0003-4761-5996"},{"first_name":"Markus","last_name":"Brown","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","full_name":"Brown, Markus"},{"full_name":"Ludewig, Burkhard","last_name":"Ludewig","first_name":"Burkhard"},{"orcid":"0000-0003-2279-1061","first_name":"Simon","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Heisenberg","full_name":"Heisenberg, Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0912-4566","first_name":"Carl-Philipp J"},{"full_name":"Weninger, Wolfgang","last_name":"Weninger","first_name":"Wolfgang"},{"orcid":"0000-0001-6005-1561","first_name":"Edouard B","last_name":"Hannezo","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","full_name":"Hannezo, Edouard B"},{"full_name":"Luther, Sanjiv A.","last_name":"Luther","first_name":"Sanjiv A."},{"first_name":"Jens V.","last_name":"Stein","full_name":"Stein, Jens V."},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","orcid":"0000-0002-4561-241X"}],"date_created":"2021-08-06T09:09:11Z","article_type":"original","volume":23,"language":[{"iso":"eng"}],"oa":1,"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"mla":"Assen, Frank P., et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” <i>Nature Immunology</i>, vol. 23, Springer Nature, 2022, pp. 1246–55, doi:<a href=\"https://doi.org/10.1038/s41590-022-01257-4\">10.1038/s41590-022-01257-4</a>.","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. <i>Nature Immunology</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41590-022-01257-4\">https://doi.org/10.1038/s41590-022-01257-4</a>","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.","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.” <i>Nature Immunology</i>. Springer Nature, 2022. <a href=\"https://doi.org/10.1038/s41590-022-01257-4\">https://doi.org/10.1038/s41590-022-01257-4</a>.","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.","ieee":"F. P. Assen <i>et al.</i>, “Multitier mechanics control stromal adaptations in swelling lymph nodes,” <i>Nature Immunology</i>, vol. 23. Springer Nature, pp. 1246–1255, 2022.","ama":"Assen FP, Abe J, Hons M, et al. Multitier mechanics control stromal adaptations in swelling lymph nodes. <i>Nature Immunology</i>. 2022;23:1246-1255. doi:<a href=\"https://doi.org/10.1038/s41590-022-01257-4\">10.1038/s41590-022-01257-4</a>"},"month":"07","file":[{"relation":"main_file","checksum":"628e7b49809f22c75b428842efe70c68","file_name":"2022_NatureImmunology_Assen.pdf","success":1,"content_type":"application/pdf","access_level":"open_access","file_id":"11642","date_created":"2022-07-25T07:11:32Z","file_size":11475325,"date_updated":"2022-07-25T07:11:32Z","creator":"dernst"}],"department":[{"_id":"SiHi"},{"_id":"CaHe"},{"_id":"EdHa"},{"_id":"EM-Fac"},{"_id":"Bio"},{"_id":"MiSi"}],"ddc":["570"],"page":"1246-1255","quality_controlled":"1","publisher":"Springer Nature","article_processing_charge":"No","doi":"10.1038/s41590-022-01257-4","type":"journal_article","_id":"9794","date_updated":"2023-08-02T06:53:07Z","status":"public","publication":"Nature Immunology","project":[{"_id":"25FE9508-B435-11E9-9278-68D0E5697425","name":"Cellular navigation along spatial gradients","grant_number":"724373","call_identifier":"H2020"}],"date_published":"2022-07-11T00:00:00Z","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.","ec_funded":1,"external_id":{"isi":["000822975900002"]},"year":"2022","isi":1},{"date_published":"2021-04-05T00:00:00Z","pmid":1,"status":"public","publication":"Journal of Cell Biology","external_id":{"isi":["000626365700001"],"pmid":["33533935"]},"year":"2021","isi":1,"quality_controlled":"1","ddc":["570"],"type":"journal_article","date_updated":"2023-09-05T13:57:53Z","_id":"9094","publisher":"Rockefeller University Press","doi":"10.1083/jcb.202006081","article_processing_charge":"No","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","issue":"4","citation":{"chicago":"Leithner, Alexander F, LM Altenburger, R Hauschild, Frank P Assen, K Rottner, Stradal TEB, A Diz-Muñoz, JV Stein, and Michael K Sixt. “Dendritic Cell Actin Dynamics Control Contact Duration and Priming Efficiency at the Immunological Synapse.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2021. <a href=\"https://doi.org/10.1083/jcb.202006081\">https://doi.org/10.1083/jcb.202006081</a>.","ista":"Leithner AF, Altenburger L, Hauschild R, Assen FP, Rottner K, TEB S, Diz-Muñoz A, Stein J, Sixt MK. 2021. Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. Journal of Cell Biology. 220(4), e202006081.","mla":"Leithner, Alexander F., et al. “Dendritic Cell Actin Dynamics Control Contact Duration and Priming Efficiency at the Immunological Synapse.” <i>Journal of Cell Biology</i>, vol. 220, no. 4, e202006081, Rockefeller University Press, 2021, doi:<a href=\"https://doi.org/10.1083/jcb.202006081\">10.1083/jcb.202006081</a>.","apa":"Leithner, A. F., Altenburger, L., Hauschild, R., Assen, F. P., Rottner, K., TEB, S., … Sixt, M. K. (2021). Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.202006081\">https://doi.org/10.1083/jcb.202006081</a>","ama":"Leithner AF, Altenburger L, Hauschild R, et al. Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. <i>Journal of Cell Biology</i>. 2021;220(4). doi:<a href=\"https://doi.org/10.1083/jcb.202006081\">10.1083/jcb.202006081</a>","short":"A.F. Leithner, L. Altenburger, R. Hauschild, F.P. Assen, K. Rottner, S. TEB, A. Diz-Muñoz, J. Stein, M.K. Sixt, Journal of Cell Biology 220 (2021).","ieee":"A. F. Leithner <i>et al.</i>, “Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse,” <i>Journal of Cell Biology</i>, vol. 220, no. 4. Rockefeller University Press, 2021."},"language":[{"iso":"eng"}],"oa":1,"file":[{"file_size":5102328,"date_created":"2022-05-12T14:16:21Z","date_updated":"2022-05-12T14:16:21Z","creator":"dernst","file_id":"11367","success":1,"file_name":"2021_JournCellBiology_Leithner.pdf","access_level":"open_access","content_type":"application/pdf","relation":"main_file","checksum":"843ebc153847c8626e13c9c5ce71d533"}],"article_number":"e202006081","department":[{"_id":"MiSi"}],"month":"04","publication_status":"published","publication_identifier":{"issn":["0021-9525"],"eissn":["1540-8140"]},"file_date_updated":"2022-05-12T14:16:21Z","tmp":{"image":"/images/cc_by_nc_sa.png","name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","short":"CC BY-NC-SA (4.0)"},"license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","abstract":[{"text":"Dendritic cells (DCs) are crucial for the priming of naive T cells and the initiation of adaptive immunity. Priming is initiated at a heterologous cell–cell contact, the immunological synapse (IS). While it is established that F-actin dynamics regulates signaling at the T cell side of the contact, little is known about the cytoskeletal contribution on the DC side. Here, we show that the DC actin cytoskeleton is decisive for the formation of a multifocal synaptic structure, which correlates with T cell priming efficiency. DC actin at the IS appears in transient foci that are dynamized by the WAVE regulatory complex (WRC). The absence of the WRC in DCs leads to stabilized contacts with T cells, caused by an increase in ICAM1-integrin–mediated cell–cell adhesion. This results in lower numbers of activated and proliferating T cells, demonstrating an important role for DC actin in the regulation of immune synapse functionality.","lang":"eng"}],"intvolume":"       220","has_accepted_license":"1","article_type":"original","date_created":"2021-02-05T10:08:04Z","volume":220,"title":"Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse","oa_version":"Published Version","author":[{"id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","full_name":"Leithner, Alexander F","last_name":"Leithner","orcid":"0000-0002-1073-744X","first_name":"Alexander F"},{"first_name":"LM","full_name":"Altenburger, LM","last_name":"Altenburger"},{"first_name":"R","full_name":"Hauschild, R","last_name":"Hauschild"},{"last_name":"Assen","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","full_name":"Assen, Frank P","first_name":"Frank P","orcid":"0000-0003-3470-6119"},{"first_name":"K","last_name":"Rottner","full_name":"Rottner, K"},{"first_name":"Stradal","last_name":"TEB","full_name":"TEB, Stradal"},{"full_name":"Diz-Muñoz, A","last_name":"Diz-Muñoz","first_name":"A"},{"first_name":"JV","full_name":"Stein, JV","last_name":"Stein"},{"orcid":"0000-0002-6620-9179","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"scopus_import":"1","day":"05"},{"month":"10","supervisor":[{"orcid":"0000-0002-6620-9179","first_name":"Michael K","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt"}],"file":[{"file_name":"PhDthesis_FrankAssen_revised2.docx","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","access_level":"closed","relation":"source_file","checksum":"53a739752a500f84d0f8ec953cbbd0b6","date_created":"2019-11-06T12:30:02Z","file_size":214172667,"creator":"fassen","date_updated":"2020-11-07T23:30:03Z","file_id":"6990","embargo_to":"open_access"},{"date_created":"2019-11-06T12:30:57Z","file_size":83637532,"embargo":"2020-11-06","date_updated":"2020-11-07T23:30:03Z","creator":"fassen","file_id":"6991","file_name":"PhDthesis_FrankAssen_revised2.pdf","content_type":"application/pdf","access_level":"open_access","relation":"main_file","checksum":"8c156b65d9347bb599623a4b09f15d15"}],"department":[{"_id":"MiSi"}],"language":[{"iso":"eng"}],"oa":1,"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"ista":"Assen FP. 2019. Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking. Institute of Science and Technology Austria.","chicago":"Assen, Frank P. “Lymph Node Mechanics: Deciphering the Interplay between Stroma Contractility, Morphology and Lymphocyte Trafficking.” Institute of Science and Technology Austria, 2019. <a href=\"https://doi.org/10.15479/AT:ISTA:6947\">https://doi.org/10.15479/AT:ISTA:6947</a>.","mla":"Assen, Frank P. <i>Lymph Node Mechanics: Deciphering the Interplay between Stroma Contractility, Morphology and Lymphocyte Trafficking</i>. Institute of Science and Technology Austria, 2019, doi:<a href=\"https://doi.org/10.15479/AT:ISTA:6947\">10.15479/AT:ISTA:6947</a>.","apa":"Assen, F. P. (2019). <i>Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking</i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/AT:ISTA:6947\">https://doi.org/10.15479/AT:ISTA:6947</a>","ama":"Assen FP. Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking. 2019. doi:<a href=\"https://doi.org/10.15479/AT:ISTA:6947\">10.15479/AT:ISTA:6947</a>","short":"F.P. Assen, Lymph Node Mechanics: Deciphering the Interplay between Stroma Contractility, Morphology and Lymphocyte Trafficking, Institute of Science and Technology Austria, 2019.","ieee":"F. P. Assen, “Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking,” Institute of Science and Technology Austria, 2019."},"title":"Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking","oa_version":"Published Version","day":"9","author":[{"last_name":"Assen","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","full_name":"Assen, Frank P","orcid":"0000-0003-3470-6119","first_name":"Frank P"}],"date_created":"2019-10-14T16:54:52Z","acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"abstract":[{"lang":"eng","text":"Lymph nodes  are es s ential organs  of the immune  s ys tem where adaptive immune responses originate, and consist of various leukocyte populations and a stromal backbone. Fibroblastic reticular  cells (FRCs) are  the  main  stromal  cells and  form  a sponge-like extracellular matrix network,   called  conduits ,  which  they   thems elves   enwrap   and  contract.  Lymph,  containing  s oluble  antigens ,  arrive in  lymph  nodes  via afferent lymphatic  vessels that  connect  to  the  s ubcaps ular  s inus   and  conduit  network.  According  to  the  current  paradigm,  the  conduit  network   dis tributes   afferent  lymph  through   lymph  nodes   and  thus   provides   acces s   for  immune  cells to lymph-borne  antigens. An  elas tic  caps ule  s urrounds   the  organ  and  confines   the immune  cells and  FRC  network.   Lymph   nodes   are  completely  packed  with  lymphocytes   and  lymphocyte  numbers  directly  dictates  the size  of  the  organ.  Although  lymphocytes   cons tantly  enter  and  leave  the  lymph  node,  its   s ize  remains   remarkedly   s table  under  homeostatic conditions. It is only partly known  how the cellularity and s ize of the lymph node is regulated and  how  the  lymph  node  is able to swell in inflammation.  The role of the FRC network   in  lymph  node   s welling  and  trans fer  of  fluids   are  inves tigated in  this   thes is.  Furthermore,   we  s tudied  what  trafficking  routes   are  us ed  by  cancer  cells   in  lymph  nodes   to  form  distal metastases.We examined the role of a mechanical feedback in regulation of lymph  node swelling. Using parallel plate compression  and UV-las er  cutting  experiments   we  dis s ected  the  mechanical  force dynamics  of the whole lymph  node, and individually for FRCs  and the  caps ule. Physical forces   generated  by  packed  lymphocytes   directly  affect  the  tens ion  on  the  FRC  network  and  capsule,  which  increases  its  resistance  to   swelling.  This  implies  a  feedback  mechanism  between   tis s ue   pres s ure   and   ability   of   lymphocytes    to   enter   the   organ.   Following   inflammation,  the  lymph  node  swells ∼10 fold in two weeks . Yet, what  is  the role  for tens ion on  the  FRC  network   and  caps ule,  and  how  are  lymphocytes   able  to  enter  in  conditions  that resist swelling remain open ques tions . We s how that tens ion on the FRC network is  important to  limit  the  swelling  rate  of  the  organ  so  that  the  FRC  network  can  grow  in  a  coordinated  fashion. This is illustrated by interfering with FRC contractility, which leads to faster swelling rates  and a dis organized FRC network  in the inflamed lymph  node. Growth  of the FRC network  in  turn  is   expected  to  releas e  tens ion  on  thes e  s tructures   and  lowers   the  res is tance  to  swelling, thereby allowing more lymphocytes to enter the organ and drive more swelling. Halt of  swelling coincides   with  a  thickening  of  the  caps ule,  which  forms   a  thick  res is tant  band  around  the organ and lowers  tens ion on the FRC network  to form a new force equilibrium.The  FRC  and  conduit   network   are  further   believed  to  be  a  privileged  s ite  of  s oluble  information  within  the  lymph  node,  although  many  details   remain  uns olved.  We  s how  by  3D  ultra-recons truction   that  FRCs   and  antigen  pres enting  cells   cover  the  s urface  of  conduit  s ys tem for more  than 99% and we dis cus s  the implications  for s oluble information  exchangeat the conduit level.Finally, there  is an ongoing debate in the cancer field whether and how cancer cells  in lymph nodes   s eed  dis tal  metas tas es .  We  s how  that  cancer  cells   infus ed  into  the  lymph  node  can  utilize trafficking routes of immune  cells and  rapidly  migrate  to  blood  vessels. Once  in  the  blood circulation,  these cells are able to form  metastases in distal tissues."}],"has_accepted_license":"1","file_date_updated":"2020-11-07T23:30:03Z","publication_identifier":{"issn":["2663-337X"]},"publication_status":"published","related_material":{"record":[{"id":"664","status":"public","relation":"part_of_dissertation"},{"id":"402","status":"public","relation":"part_of_dissertation"}]},"year":"2019","status":"public","degree_awarded":"PhD","date_published":"2019-10-09T00:00:00Z","publisher":"Institute of Science and Technology Austria","article_processing_charge":"No","alternative_title":["ISTA Thesis"],"doi":"10.15479/AT:ISTA:6947","type":"dissertation","_id":"6947","date_updated":"2023-09-13T08:50:57Z","ddc":["570"],"page":"142"},{"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.","date_published":"2018-03-23T00:00:00Z","pmid":1,"ec_funded":1,"project":[{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12"},{"_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"}],"publication":"Science","status":"public","publist_id":"7428","external_id":{"pmid":["29567714"],"isi":["000428043600047"]},"related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"6947"}]},"isi":1,"year":"2018","quality_controlled":"1","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1126/science.aal3662"}],"page":"1408 - 1411","type":"journal_article","date_updated":"2024-03-25T23:30:05Z","_id":"402","publisher":"American Association for the Advancement of Science","doi":"10.1126/science.aal3662","article_processing_charge":"No","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","issue":"6382","citation":{"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.” <i>Science</i>. American Association for the Advancement of Science, 2018. <a href=\"https://doi.org/10.1126/science.aal3662\">https://doi.org/10.1126/science.aal3662</a>.","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.","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. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.aal3662\">https://doi.org/10.1126/science.aal3662</a>","mla":"Brown, Markus, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” <i>Science</i>, vol. 359, no. 6382, American Association for the Advancement of Science, 2018, pp. 1408–11, doi:<a href=\"https://doi.org/10.1126/science.aal3662\">10.1126/science.aal3662</a>.","ama":"Brown M, Assen FP, Leithner AF, et al. Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. <i>Science</i>. 2018;359(6382):1408-1411. doi:<a href=\"https://doi.org/10.1126/science.aal3662\">10.1126/science.aal3662</a>","ieee":"M. Brown <i>et al.</i>, “Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice,” <i>Science</i>, vol. 359, no. 6382. American Association for the Advancement of Science, pp. 1408–1411, 2018.","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."},"language":[{"iso":"eng"}],"oa":1,"department":[{"_id":"MiSi"}],"month":"03","publication_status":"published","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."}],"intvolume":"       359","acknowledged_ssus":[{"_id":"Bio"}],"article_type":"original","date_created":"2018-12-11T11:46:16Z","volume":359,"title":"Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice","oa_version":"Published Version","author":[{"id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","full_name":"Brown, Markus","last_name":"Brown","first_name":"Markus"},{"orcid":"0000-0003-3470-6119","first_name":"Frank P","last_name":"Assen","full_name":"Assen, Frank P","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Alexander F","orcid":"0000-0002-1073-744X","last_name":"Leithner","full_name":"Leithner, Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Abe, Jun","last_name":"Abe","first_name":"Jun"},{"full_name":"Schachner, Helga","last_name":"Schachner","first_name":"Helga"},{"full_name":"Asfour, Gabriele","last_name":"Asfour","first_name":"Gabriele"},{"first_name":"Zsuzsanna","last_name":"Bagó Horváth","full_name":"Bagó Horváth, Zsuzsanna"},{"last_name":"Stein","full_name":"Stein, Jens","first_name":"Jens"},{"first_name":"Pavel","full_name":"Uhrin, Pavel","last_name":"Uhrin"},{"first_name":"Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K"},{"full_name":"Kerjaschki, Dontscho","last_name":"Kerjaschki","first_name":"Dontscho"}],"day":"23","scopus_import":"1"},{"abstract":[{"text":"Immune cells communicate using cytokine signals, but the quantitative rules of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et al. (2017) suggest that the distribution of a cytokine within a lymphatic organ is primarily governed by the local density of cells consuming it.","lang":"eng"}],"intvolume":"        46","page":"519 - 520","publication_status":"published","publication_identifier":{"issn":["10747613"]},"quality_controlled":"1","publisher":"Cell Press","oa_version":"None","title":"The dynamic cytokine niche","scopus_import":1,"day":"18","author":[{"orcid":"0000-0003-3470-6119","first_name":"Frank P","last_name":"Assen","full_name":"Assen, Frank P","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","first_name":"Michael K"}],"doi":"10.1016/j.immuni.2017.04.006","date_created":"2018-12-11T11:47:47Z","type":"journal_article","_id":"664","volume":46,"date_updated":"2024-03-25T23:30:05Z","status":"public","language":[{"iso":"eng"}],"publication":"Immunity","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","date_published":"2017-04-18T00:00:00Z","citation":{"mla":"Assen, Frank P., and Michael K. Sixt. “The Dynamic Cytokine Niche.” <i>Immunity</i>, vol. 46, no. 4, Cell Press, 2017, pp. 519–20, doi:<a href=\"https://doi.org/10.1016/j.immuni.2017.04.006\">10.1016/j.immuni.2017.04.006</a>.","apa":"Assen, F. P., &#38; Sixt, M. K. (2017). The dynamic cytokine niche. <i>Immunity</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.immuni.2017.04.006\">https://doi.org/10.1016/j.immuni.2017.04.006</a>","chicago":"Assen, Frank P, and Michael K Sixt. “The Dynamic Cytokine Niche.” <i>Immunity</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.immuni.2017.04.006\">https://doi.org/10.1016/j.immuni.2017.04.006</a>.","ista":"Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520.","short":"F.P. Assen, M.K. Sixt, Immunity 46 (2017) 519–520.","ieee":"F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” <i>Immunity</i>, vol. 46, no. 4. Cell Press, pp. 519–520, 2017.","ama":"Assen FP, Sixt MK. The dynamic cytokine niche. <i>Immunity</i>. 2017;46(4):519-520. doi:<a href=\"https://doi.org/10.1016/j.immuni.2017.04.006\">10.1016/j.immuni.2017.04.006</a>"},"issue":"4","month":"04","related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"6947"}]},"year":"2017","publist_id":"7065","department":[{"_id":"MiSi"}]}]