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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Control of target cell survival in thyroid autoimmunity by T helper cytokines via regulation of apoptotic proteins.

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 TH1 and TH2 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-xL, which prevented CD95-induced apoptosis in sensitized thyrocytes. Thus, modulation of apoptosis-related proteins by TH1 and TH2 cytokines controls thyrocyte survival in thyroid autoimmunity.[1]

References

  1. Control of target cell survival in thyroid autoimmunity by T helper cytokines via regulation of apoptotic proteins. Stassi, G., Di Liberto, D., Todaro, M., Zeuner, A., Ricci-Vitiani, L., Stoppacciaro, A., Ruco, L., Farina, F., Zummo, G., De Maria, R. Nat. Immunol. (2000) [Pubmed]
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