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ShareMar. 1, 2010 — Using a mouse model of type 1 diabetes, Lisa Denzin and colleagues, at Sloan-Kettering Institute, New York, have clearly defined the in vivo biological role of the immune system protein DO, something that had not been well characterized before.
Immune cells known as CD4+ T cells are triggered to mount a response when they recognize a peptide in association with a protein complex known as MHCII. The peptide repertoire associated with MHCII therefore has a key role in determining what CD4+ T cells are triggered. If a CD4+ T cell recognizes an MHCII complex associated with peptides derived from proteins in the body then the CD4+ T cell is triggered to attack the body, leading to autoimmune diseases such as type 1 diabetes.
In their study, Denzin and colleagues provide clear evidence to support the hypothesis that the protein DO modulates the repertoire of peptides associated with MHCII such that fewer of the peptides are derived from proteins in the body and thus the development of autoimmunity is suppressed.
The researchers therefore suggest that modulating the MHCII-associated peptide repertoire might provide a way to treat and/or prevent autoimmune disease.
The research appears in the Journal of Clinical Investigation.
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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
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Journal Reference:
- woelsung Yi, Nilufer P. Seth, Tom Martillotti, Kai W. Wucherpfennig, Derek B. Sant%u2019angelo, and Lisa K. Denzin. Targeted regulation of self-peptide presentation prevents type I diabetes in mice without disrupting general immunocompetence. Journal of Clinical Investigation, 2010; DOI: 10.1172/JCI40220
Note: If no author is given, the source is cited instead.
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