Peptide specific amelioration of T cell mediated pathogenesis in murine type 1 diabetes Article

Judkowski, V, Rodriguez, E, Pinilla, C et al. (2004). Peptide specific amelioration of T cell mediated pathogenesis in murine type 1 diabetes . 113(1), 29-37. 10.1016/j.clim.2004.03.007

cited authors

  • Judkowski, V; Rodriguez, E; Pinilla, C; Masteller, E; Bluestone, JA; Sarvetnick, N; Wilson, DB

authors

abstract

  • NOD mice spontaneously develop insulitis and type 1 diabetes (T1D) mellitus similar to humans. Insulitis without overt disease occurs in the BDC2.5 TCR-transgenic NOD mice that express the rearranged TCR α- and β-chain genes of a diabetogenic T cell clone reactive to an unknown β cell autoantigen. A previous study identified an extensive panel of peptides that are highly active in stimulating T cells from transgenic BDC2.5 mice in culture. However, none of these peptides cause active disease in NOD and BDC2.5 animals or in NOD recipients of adoptively transferred BDC2.5 T cells following direct immunization in vivo. We show that direct immunization of transgenic BDC2.5 mice causes many BDC2.5 T cells to become activated and apoptotic. Strikingly, soluble peptides administered to recipients of activated, highly pathogenic BDC2.5 T cells results in protection from disease. These results suggest that high affinity peptide analogues of autoimmune epitopes might be useful as therapeutic modulators in active autoimmune disease. © 2004 Elsevier Inc. All rights reserved.

publication date

  • October 1, 2004

Digital Object Identifier (DOI)

start page

  • 29

end page

  • 37

volume

  • 113

issue

  • 1