Journal
NATURE IMMUNOLOGY
Volume 6, Issue 7, Pages 715-721Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1211
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Funding
- NIAID NIH HHS [AI21372-20, AI37988-09] Funding Source: Medline
- NIDDK NIH HHS [5T32DK07233] Funding Source: Medline
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Suppressor of cytokine signaling 1 (Socs1) is critical for the regulation of interferon-c responses and T cell homeostasis. Although the presentation of the inflammatory disease of Socs1-deficient mice is complex, we have tested here the hypothesis that it originates from inappropriate T cell development and the appearance of autoreactive T cells. Socs1-deficient T cell receptor-transgenic mice showed severely impaired positive selection and a substantial alteration in CD4-CD8 T cell fate specification. These defects were dependent on interferon-gamma. Moreover, negative selection was also impaired, suggesting that autoimmunity contributes to the disease observed in Socs1(-/-) mice. We conclude that the constitutive expression of Socs1 in the thymus protects the process of thymic development and selection from the effects of systemic inflammation.
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