Impaired activation‐induced cell death promotes spontaneous arthritis in antigen (cartilage proteoglycan)–specific T cell receptor–transgenic mice

Abstract

The presence of CD4+ T cells expressing a TCR specific for an arthritogenic PG epitope is sufficient to trigger spontaneous autoimmune inflammation in the joints of BALB/c mice. IL-4 appears to be a negative regulator of this disease, through attenuation of activation-induced cell death.