J Neuroimmunol 2002 Feb;123(1-2):112-22
Song F, Gienapp IE, Wang X, Whitacre CC.
Department of Molecular Virology, Immunology and Medical Genetics, College of Medicine and Public Health, The Ohio State University, 2078 Graves Hall, 333 West 10th Avenue, 43210, Columbus, OH, USA
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.