期刊
JOURNAL OF IMMUNOLOGY
卷 173, 期 3, 页码 1658-1662出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.173.3.1658
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- NIAID NIH HHS [R01-AI44835] Funding Source: Medline
Wiskott-Aldrich syndrome protein (WASP)-deficient T cells exhibit defects in IL-2 production that are widely believed to stem from primary defects in actin remodeling and immune synapse formation. Surprisingly, however, we find that WASP-deficient T cells responding to Ag-specific APCs polymerize actin and organize talin and PKCtheta normally, forming an immune synapse that is stable for at least 3 h. At low doses of peptide, WASP-deficient T cells show less efficient talin and PKCtheta polarization. Thus, although WASP may facilitate immune synapse formation at low peptide concentrations, WASP is not required for this process. Defects in IL-2 production are observed even under conditions in which immune synapse formation proceeds normally, suggesting that the role of WASP in regulating IL-2 production is independent of its role in immune synapse formation.
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