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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.

Author information

1
Department of Immunology and Infectious Disease, John Curtin School of Medical Research, The Australian National University, Canberra, ACT 2602, Australia.
2
Department of Microbiology, University of Tennessee, Knoxville, Tennessee, United States of America.
3
Department of Microbiology and Immunology, The Peter Doherty Institute, University of Melbourne, Parkville, VIC 3010, Australia.
4
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.
5
Immunogenomics Laboratory, Garvan Institute of Medical Research, Darlinghurst, Sydney, NSW 2010, Australia.

Abstract

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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