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LFA-1 in T cell priming, differentiation, and effector functions
被引:52
|作者:
Gerard, Audrey
[1
]
Cope, Andrew P.
[2
]
Kemper, Claudia
[3
,4
]
Alon, Ronen
[5
]
Kochl, Robert
[6
]
机构:
[1] Univ Oxford, Kennedy Inst Rheumatol, Oxford, England
[2] Kings Coll London, Ctr Inflammat Biol & Canc Immunol, London, England
[3] NHLBI, NIH, CIRS, Bldg 10, Bethesda, MD 20892 USA
[4] Univ Lubeck, Inst System Inflammat Res, Lubeck, Germany
[5] Weizmann Inst Sci, Rehovot, Israel
[6] Kings Coll London, Peter Gorer Dept Immunobiol, London, England
基金:
英国惠康基金;
英国生物技术与生命科学研究理事会;
以色列科学基金会;
关键词:
ANTIGEN-PRESENTING CELLS;
COFACTOR PROTEIN CD46;
DENDRITIC CELLS;
LYMPH-NODES;
IN-VIVO;
IMMUNOLOGICAL SYNAPSE;
ADHESION MOLECULE;
IMMUNE-RESPONSE;
ACTIVATION;
COMPLEMENT;
D O I:
10.1016/j.it.2021.06.004
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
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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页码:706 / 722
页数:17
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