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

期刊

TRENDS IN IMMUNOLOGY
卷 42, 期 8, 页码 706-722

出版社

CELL PRESS
DOI: 10.1016/j.it.2021.06.004

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资金

  1. Kennedy Trust for Rheumatology Research [KENN151607]
  2. BBSRC [BB/R015651/1]
  3. Cancer Research UK [C65275/A29549]
  4. Arthritis Research UK [19652, 20525]
  5. Royal Society
  6. Wellcome Trust [086054]
  7. Israel Science Foundation [791/17]
  8. Minerva Foundation
  9. ERA-Net ERare3
  10. GIF [I1470412.13/2018]
  11. Division of Intramural Research of the National Heart, Lung, and Blood Institute, NIH
  12. Academy of Medical Sciences Springboard award [SBF006\1100]
  13. BBSRC [BB/R015651/1] Funding Source: UKRI

向作者/读者索取更多资源

The integrin LFA-1 plays a crucial role in T cell entry into lymph nodes and tissues, interactions with antigen-presenting cells, as well as additional functions such as T-T communication and support of T cell memory. Understanding the biology of LFA-1 and its mechanobiology is important for studying immunological synapses and pathologies related to LFA-1 dysregulation.
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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