RGD Reference Report - Induction of autoimmunity in the absence of CD28 costimulation. - Chinchilla Research Resource Database
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Induction of autoimmunity in the absence of CD28 costimulation.

Authors: Bachmaier, K  Pummerer, C  Shahinian, A  Ionescu, J  Neu, N  Mak, T W  Penninger, J M 
Citation: Bachmaier K, etal., J Immunol. 1996 Aug 15;157(4):1752-7.
CRRD ID: 13702883
Pubmed: (View Article at PubMed) PMID:8759765

Ag-specific activation of T lymphocytes requires two signals, one by the TCR and a second by costimulatory molecules. In a CD4+ T helper cell-dependent experimental autoimmune myocarditis model, we provide genetic evidence that cardiac myosin-induced autoimmune myocarditis and the production of IgG auto-Abs is dependent on functional T cells and did not occur in mice lacking the tyrosine kinase p56lck or the tyrosine phosphatase CD45. By contrast, animals lacking the T cell-costimulatory molecule CD28 (CD28 -/-) developed autoimmune heart disease, although at significantly lower severity than in heterozygous littermates, and produced IgG auto-Abs depending on the concentration of the autoantigen administered. In addition, the isotypes of IgG auto-Abs specific for cardiac myosin differed between CD28 +/- and CD28 -/- mice. Whereas CD28 +/- mice predominantly produced Th2-mediated IgG1 auto-Abs, CD28 -/- mice produced predominantly IgG2a. These data suggest that CD28 costimulation plays a crucial role in induction and maintenance of autoimmune heart disease and that CD28 expression is required for predominant Th2-IgG1 responses in an autoimmune setting.


Disease Annotations    

Objects Annotated

Genes (Homo sapiens)
CD28  (CD28 molecule)

Additional Information



RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.