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Altered regulation of IL-2 production in systemic lupus erythematosus: an evolving paradigm
Gary M. Kammer
Gary M. Kammer
Published April 1, 2005
Citation Information: J Clin Invest. 2005;115(4):836-840. https://doi.org/10.1172/JCI24791.
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Commentary

Altered regulation of IL-2 production in systemic lupus erythematosus: an evolving paradigm

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Abstract

In systemic lupus erythematosus (SLE), IL-2 production by T lymphocytes in vitro is impaired. Deficient IL-2 production may be an outcome of a primary SLE T cell disorder that is due to impaired signal transduction. In this issue of the JCI, evidence is presented that an anti-TCR/CD3 complex autoantibody present in SLE sera can bind to T cells and activate the Ca2+-calmodulin kinase IV (CaMKIV) signaling cascade, resulting in downregulation of IL-2 transcription and IL-2 production. Because IL-2 may contribute to the maintenance of T cell tolerance, deficient IL-2 production could promote a breach of T cell tolerance that results in autoantibody production in SLE.

Authors

Gary M. Kammer

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Abnormal signaling molecules in SLE T cells

Abnormal signaling molecules in SLE T cells

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