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Peptide-based treatment for autoimmune diseases: learning how to handle a double-edged sword
Alberto Pugliese
Alberto Pugliese
Published May 1, 2003
Citation Information: J Clin Invest. 2003;111(9):1280-1282. https://doi.org/10.1172/JCI18395.
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Commentary

Peptide-based treatment for autoimmune diseases: learning how to handle a double-edged sword

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Abstract

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Alberto Pugliese

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Figure 1

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Disabling a CD8+ epitope. Intranasal administration of different proinsu...
Disabling a CD8+ epitope. Intranasal administration of different proinsulin peptides results in presentation from an antigen-presenting cell (APC) to CD4+ and CD8+ T cells, depending on the peptide administered. Proinsulin peptides B24–C36, B24–C35, and B26–C34 can bind to the MHC class I molecule (Kd), resulting in the activation of cytotoxic T cells. The use of truncated peptides that do not contain the residues critical for binding to Kd, but still bind to the NOD mouse MHC class II molecule (I-Ag7), allows for selective activation of regulatory CD4+ T cells. The same APC is shown presenting simultaneously to both CD4+ and CD8+ T cells for illustration purposes. TCR, T cell receptor.

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