Journal
JOURNAL OF IMMUNOLOGY
Volume 187, Issue 12, Pages 6256-6267Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1102028
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Funding
- National Institutes of Health (NIH) [R01 CA085862]
- NIH/National Institute of Allergy and Infectious Diseases [R01 AI068062]
- University of Wisconsin Institute on Aging (NIH) [T32AG000213-17]
- Wellcome Trust
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T cell-APC contact initiates T cell activation and is maintained by the integrin LFA-1. Talin1, an LFA-1 regulator, localizes to the immune synapse (IS) with unknown roles in T cell activation. In this study, we show that talin1-deficient T cells have defects in contact-dependent T cell stopping and proliferation. Although talin1-deficient T cells did not form stable interactions with APCs, transient contacts were sufficient to induce signaling. In contrast to prior models, LFA-1 polarized to T cell-APC contacts in talin1-deficient T cells, but vinculin and F-actin polarization at the IS was impaired. These results indicate that T cell proliferation requires sustained, talin1-mediated T cell-APC interactions and that talin1 is necessary for F-actin polarization and the stability of the IS. The Journal of Immunology, 2011, 187: 6256-6267.
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