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An immunologic homunculus for type 1 diabetes
Dirk Homann, George S. Eisenbarth
Dirk Homann, George S. Eisenbarth
Published May 1, 2006
Citation Information: J Clin Invest. 2006;116(5):1212-1215. https://doi.org/10.1172/JCI28506.
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Commentary

An immunologic homunculus for type 1 diabetes

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Abstract

Autoimmune diseases such as the diabetes that develops in NOD mice depend on immunologic recognition of specific autoantigens, but recognition can result in a pathogenic or protective T cell response. A study by Du et al. in this issue of the JCI demonstrates that TGF-β signaling by T cells recognizing the insulin peptide B:9–23 is essential for such protection and that this inhibitory cytokine functions in both a paracrine and an autocrine manner (see the related article beginning on page 1360). We propose that the insulin peptide B:9–23 and a conserved TCR motif form an “immunologic homunculus” underlying the relatively common targeting of insulin by T cells that, as demonstrated by the study of Du and coworkers, results in a protective T cell response, or diabetes, as shown by other investigators, for related T cell receptors.

Authors

Dirk Homann, George S. Eisenbarth

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