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Activation of Vbeta8 T cells affects spontaneous EAE in MBP TCR transgenic mice
Fei Song1, Ingrid E Gienapp, Xianming Wang
1Department of Molecular Virology, Immunology and Medical Genetics, College of Medicine and Public Health, The Ohio State University, Columbus, OH 43210, USA.
Abstract:
Two strains of transgenic (Tg) mice (Valpha2.3/Vbeta8.2 and Valpha4/Vbeta8.2) have T cell receptors (TCR) that recognize the NAc1-11 immunodominant epitope of the myelin basic protein (MBP). Spontaneous experimental autoimmune encephalomyelitis (sEAE) readily develops in Valpha2.3/Vbeta8.2 mice. T cells in Valpha2.3/Vbeta8.2 mice demonstrate increased levels of CD69, CD44(high) and decreased CD45RB relative to Valpha4/Vbeta8.2 mice. Increased proliferative responses to MBP and high levels of TNF-alpha are seen in Valpha2.3/Vbeta8.2 mice. High IL-4 and TGF-beta production is observed in Valpha4/Vbeta8.2 mice. CC chemokines (macrophage inflammatory protein-1 alpha (MIP-1alpha), RANTES and monocyte chemotactic protein 1 (MCP-1)) are increased in the central nervous system (CNS) of Valpha2.3/Vbeta8.2 mice. Thus, activated Th1 cells in the periphery of Valpha2.3/Vbeta8.2 mice may traffic to the CNS in response to CC chemokines, influencing sEAE.