Astrocytes act as antigen-presenting cells in autoimmune encephalomyelitis.

2003 FEB 12 - (NewsRx.com & NewsRx.net) -- "The role of the MHC class II transactivator (CIITA) in antigen presentation by astrocytes and susceptibility to experimental autoimmune encephalomyelitis (EAE) was examined using CIITA-deficient mice and newly created transgenic mice that used the glial fibrillary acidic protein promoter to target CIITA expression in astrocytes. CIITA was required for class II expression on astrocytes. Like class II-deficient mice, CIITA-deficient mice were resistant to EAE by immunization with CNS autoantigen, although T cells from immunized CIITA-deficient, but not class II-deficient, mice proliferated and secreted Th1 cytokines," researchers in the United States report.

"CIITA-deficient splenic APC presented encephalitogenic peptide to purified wild-type encephalitogenic CD4+ T cells, indicating that CIITA-independent mechanisms can be used for class II-restricted antigen presentation in lymphoid tissue," reported Olaf Stuve and colleagues at the University of California in San Francisco, Stanford University, Glaxo SmithKline Pharmaceuticals, and Tularik. "CIITA-deficient mice were also resistant to EAE by adoptive transfer of encephalitogenic class II-restricted CD4+ Th1 cells, indicating that CIITA-dependent class II expression was required for CNS antigen presentation."

The investigators found that "despite constitutive CIITA-driven class II expression on astrocytes in vivo, glial fibrillary acidic protein-CIITA transgenic mice were no more susceptible to EAE than controls. CIITA-transfected astrocytes presented peptide antigen, but in contrast to ...