Journal
JOURNAL OF IMMUNOLOGY
Volume 199, Issue 4, Pages 1213-1221Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1700495
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Funding
- Lee Kong Chian School of Medicine, Nanyang Technological University Start-Up Grant
- Ministry of Education Singapore Academic Research Fund Tier 1 Grant [2014-T1-001-141]
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The alpha(L)beta(2) integrin LFA-1 is known to play a key role in T lymphocyte migration, which is necessary to mount a local immune response, and is also the main driver of autoimmune diseases. This migration-triggering signaling process in T cells is tightly regulated to permit an immune response that is appropriate to the local trigger, as well as to prevent deleterious tissue-damaging bystander effects. Emerging evidence shows that, in addition to prompting a diverse range of downstream signaling cascades, LFA-1 stimulation in T lymphocytes modulates gene-transcription programs, including genetic signatures of TGF-beta and Notch pathways, with multifactorial biological outcomes. This review highlights recent findings and discusses molecular mechanisms by which LFA-1 signaling influence T lymphocyte differentiation into the effector subsets Th1, Th17, and induced regulatory T cells. We argue that LFA-1 contact with a cognate ligand, such as ICAM-1, independent of the immune synapse activates a late divergence in T cells' effector phenotypes, hence fine-tuning their functioning.
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