J Autoimmun 2002 Feb;18(1):27-37
Song F, Wardrop RM, Gienapp IE, Stuckman SS, Goverman J, Whitacre CC.
Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University College of Medicine and Public Health, Columbus, OH 43210
Experimental autoimmune encephalomyelitis (EAE) is mediated by CD4(+) T cells which preferentially use the Vbeta8.2 TCR in response to myelin basic protein (MBP).
Two strains of Tg mice (Valpha2.3/Vbeta8.2 and Valpha4/Vbeta8.2) have T cell receptors that recognize the NAc1-11 immunodominant epitope of MBP.
We previously reported that oral administration of MBP protects both Valpha2.3/Vbeta8.2 and Valpha4/Vbeta8.2 mice from EAE; however, tolerance induction differs between strains and is dependent on the timing of oral antigen.
Here we analyze the peripheral and gut-associated lymphoid tissue (GALT) environments of the two strains of Tg mice.
Tg cells in the Peyer's patch (PP) but not the spleen of Valpha2.3/Vbeta8.2 mice demonstrate increased CD69 and decreased CD45RB relative to Valpha4/Vbeta8.2 mice.
High levels of Th1 and Th2 cytokines, proliferative activity and CC chemokines (MCP-1) are observed in the periphery and GALT of Valpha2.3/Vbeta8.2 Tg mice.
In contrast, more non-Tg CD4(+) cells are seen in the PP of Valpha4/Vbeta8.2 mice.
These studies suggest that activated
Tg T cells and fewer potential regulatory cells in the PP of Valpha2.3/Vbeta8.2
Tg mice may influence oral tolerance.
Copyright 2002 Elsevier Science Ltd.