Juvenile diabetes can result when cells of the immune system recognize and attack the pancreas. A report in the April issue of Nature Immunology shows how specific “decoys” can subvert the initial activation process by the autoreactive immune cells and block the subsequent tissue damage.
Using a model system of diabetes where the targeted self-protein, as well as the identity of the pathogenic T cells, are known, Sofia Casares and colleagues at the Mount Sinai School of Medicine developed soluble decoy molecules (DEF) that mimicked the normal cellular antigen presentation of peptides to T cells. However, T cells binding to DEF were not activated, as they normally are by peptides, but instead were made “tolerant” of this peptide. This situation led to the development of regulatory T cells that produce cytokines that inhibit pathogenic T cells from killing their targets. Importantly, soluble DEF treatment not only blocked the development of diabetes, but also could treat recent-onset disease in their experimental system, by restoring normal glucose control.
Long-term protection from diabetes was achieved by periodic administration of DEF. Thus, armed with specific knowledge of the pathogenic immune cell target and the identity of the responding cells, these experiments show the feasibility of immunospecific therapies for diabetes and possibly other autoimmune diseases.
Mount Sinai School of Medicine
New York, NY
Tel: +1 212 241 9777
Additional contact for comment on paper:
George S. Eisenbarth
University of Colorado Health Sciences Center
Tel: +1 303 315 4891
Also available as an Advanced Online Publication.
(C) Nature Immunology press release.
Message posted by: Trevor M. D'Souza