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Sci Immunol. 2017 Mar;2(9). pii: eaaj1996. doi: 10.1126/sciimmunol.aaj1996. Epub 2017 Mar 17.

Up-regulation of LFA-1 allows liver-resident memory T cells to patrol and remain in the hepatic sinusoids.

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Department of Immunology and Infectious Disease, John Curtin School of Medical Research, The Australian National University, Canberra, ACT 2602, Australia.
Department of Microbiology, University of Tennessee, Knoxville, Tennessee, United States of America.
Department of Microbiology and Immunology, The Peter Doherty Institute, University of Melbourne, Parkville, VIC 3010, Australia.
Liver Immunology Program, Centenary Institute and AW Morrow Gastroenterology and Liver Centre, University of Sydney and Royal Prince Alfred Hospital, Locked Bag No. 6, Sydney, NSW 2042, Australia.
Immunogenomics Laboratory, Garvan Institute of Medical Research, Darlinghurst, Sydney, NSW 2010, Australia.


Liver-resident CD8+ T cells are highly motile cells that patrol the vasculature and provide protection against liver pathogens. A key question is: how can these liver CD8+ T cells be simultaneously present in the circulation and tissue-resident? Because liver-resident T cells do not express CD103 - a key integrin for T cell residence in epithelial tissues - we investigated other candidate adhesion molecules. Using intra-vital imaging we found that CD8+ T cell patrolling in the hepatic sinusoids is dependent upon LFA-1-ICAM-1 interactions. Interestingly, liver-resident CD8+ T cells up-regulate LFA-1 compared to effector-memory cells, presumably to facilitate this behavior. Finally, we found that LFA-1 deficient CD8+ T cells failed to form substantial liver-resident memory populations following Plasmodium or LCMV immunization. Collectively, our results demonstrate that it is adhesion through LFA-1 that allows liver-resident memory CD8+ T cells to patrol and remain in the hepatic sinusoids.

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