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PMID:16339515
| Citation |
Srivatsan, S and Peng, SL (2005) Cutting edge: Foxj1 protects against autoimmunity and inhibits thymocyte egress. J. Immunol. 175:7805-9 |
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| Abstract |
Previous studies suggest that the forkhead transcription factor Foxj1 inhibits spontaneous autoimmunity in part by antagonizing NF-kappaB activation. To test this hypothesis, we ectopically expressed Foxj1 in the T cells of lupus-prone MRL/lpr mice by backcrossing a CD2-Foxj1 transgene against the MRL/lpr background. Strikingly, CD2-Foxj1-MRL/lpr animals showed a significant reduction in lymphadenopathy, pathogenic autoantibodies, and end-organ disease-but surprisingly, reversion of autoimmunity was not attributable to modulation of NF-kappaB. Instead, CD2-Foxj1 transgenic mice exhibited a peripheral T cell lymphopenia, associated with an accumulation of mature single-positive thymocytes. Transgenic thymocytes demonstrated unimpaired lymphoid organ entry in adoptive transfer studies but demonstrated impaired thymic exodus in response to CCL19, apparently independent of CCR7, S1P1, and NF-kappaB. These findings confirm the importance of Foxj1 in the regulation of T cell tolerance but furthermore suggest a novel and specific role for Foxj1 in regulating thymic egress. |
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| Keywords |
Adoptive Transfer; Animals; Antigens, CD2/genetics; Autoimmunity; Chemokine CCL19; Chemokines, CC; Chemotaxis, Leukocyte; Forkhead Transcription Factors/genetics; Forkhead Transcription Factors/physiology; Humans; Immune Tolerance; Lymphopenia/etiology; Mice; Mice, Transgenic; T-Lymphocytes/metabolism; T-Lymphocytes/physiology; Thymus Gland/cytology |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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