期刊
IMMUNITY
卷 28, 期 1, 页码 40-51出版社
CELL PRESS
DOI: 10.1016/j.immuni.2007.11.023
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资金
- NIAID NIH HHS [AI051977] Funding Source: Medline
- NIAMS NIH HHS [R01 AR042242, AR31203, R01 AR039555-13, R01 AR039555, AR42242, R37 AR039555, R01 AR031203, AR39555, R01 AR031203-24] Funding Source: Medline
- NIGMS NIH HHS [GM65230, R01 GM065230] Funding Source: Medline
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR031203, R01AR042242, R37AR039555, R01AR039555] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM065230] Funding Source: NIH RePORTER
Here, we show that a lupus-suppressing locus is caused by a nonsense mutation of the filamentous actin-inhibiting Coronin-1A gene. This mutation was associated with developmental and functional Alterations in T cells including reduced migration, survival, activation, and Ca2+ flux. T-dependent humoral responses were impaired, but no intrinsic B cell defects were detected. By transfer of T cells, it was shown that suppression of autoimmunity could be accounted for by the presence of the Coro1a(Lmb3) mutation in T cells. Our results demonstrate that Coronin-1A is required for the development of systemic lupus and identify actin-cytoskeleton regulatory proteins as potential targets for modulating autoimmune diseases.
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