Journal
NATURE IMMUNOLOGY
Volume 1, Issue 6, Pages 483-488Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/82725
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- Telethon [E.0735] Funding Source: Medline
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After autoimmune inflammation, interactions between CD95 and its ligand (CD95L) mediate thyrocyte destruction in Hashimoto's thyroiditis (HT). Conversely, thyroid autoimmune processes that lead to Graves' disease (GD) result in autoantibody-mediated thyrotropin receptor stimulation without thyrocyte depletion,We found that GD thyrocytes expressed CD95 and CD95L in a similar manner to HT thyrocytes, but did not undergo CD95-induced apoptosis either in vivo or in vitro. This pattern was due to the differential production of T(H)1 and T(H)2 cytokines. Interferon gamma promoted caspase up-regulation and CD95-induced apoptosis in HT thyrocytes, whereas interleukin 4 and interleukin 10 protected GD thyrocytes by potent up-regulation of cFLIP and Bcl-x(L), which prevented CD95-induced apoptosis in sensitized thyrocytes. Thus, modulation of apoptosis-related proteins by T(H)1 and T(H)2 cytokines controls thyrocyte survival in thyroid autoimmunity.
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