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LFA-1 in T cell priming, differentiation, and effector functions

Research output: Contribution to journalReview articlepeer-review

Audrey Gérard, Andrew P. Cope, Claudia Kemper, Ronen Alon, Robert Köchl

Original languageEnglish
Pages (from-to)706-722
Number of pages17
Issue number8
PublishedAug 2021

Bibliographical note

Funding Information: The research described in this review was supported by: the Kennedy Trust for Rheumatology Research ( KENN151607 ), the BBSRC ( BB/R015651/1 ), and Cancer Research UK ( C65275/A29549 ) (to A.G); Arthritis Research UK grants 19652 and 20525 , a Royal Society collaborative travel grant , and a Wellcome Trust project grant 086054 (to A.P.C.); the Israel Science Foundation (grant no. 791/17 ), the Minerva Foundation , ERA-Net E-Rare-3 , and GIF (grant number I-1470-412.13/2018 ) (to R.A.); the Division of Intramural Research of the National Heart, Lung, and Blood Institute , NIH (to C.K.); and the Academy of Medical Sciences Springboard award ( SBF006\1100 ) (to R.K.). Publisher Copyright: © 2021 Copyright: Copyright 2021 Elsevier B.V., All rights reserved.

King's Authors


The integrin LFA-1 is crucial for T cell entry into mammalian lymph nodes and tissues, and for promoting interactions with antigen-presenting cells (APCs). However, it is increasingly evident that LFA-1 has additional key roles beyond the mere support of adhesion between T cells, the endothelium, and/or APCs. These include roles in homotypic T cell–T cell (T–T) communication, the induction of intracellular complement activity underlying Th1 effector cell polarization, and the support of long-lasting T cell memory. Here, we briefly summarize current knowledge of LFA-1 biology, discuss novel cytoskeletal regulators of LFA-1 functions, and review new aspects of LFA-1 mechanobiology that are relevant to its function in immunological synapses and in specific pathologies arising from LFA-1 dysregulation.

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