Accelerated thymocyte maturation in IL-12Rβ2-deficient mice contributes to increased susceptibility to autoimmune inflammatory demyelination.

Abstract:

:IL-12Rβ2(-/-) mice, which are unresponsive to IL-12, develop severe experimental autoimmune encephalomyelitis (EAE). The mechanisms for enhanced autoimmunity are incompletely understood. We report that in IL-12Rβ2(-/-) mice, thymocytes undergo markedly accelerated maturation. This occurs at the transition from a double positive (DP) to a single positive (SP) phenotype, resulting in higher numbers of CD4 and CD8 SP cells, and to a lesser extent at the transition from double negative (DN) to DP cells. Accelerated maturation is observed in mice injected with anti-CD3 to mimic pre-T-cell receptor stimulation, and also in mice immunized with myelin oligodendrocyte glycoprotein (MOG) peptide to induce EAE.

journal_name

Exp Mol Pathol

authors

Gran B,Yu S,Zhang GX,Rostami A

doi

10.1016/j.yexmp.2010.06.003

subject

Has Abstract

pub_date

2010-10-01 00:00:00

pages

126-34

issue

2

eissn

0014-4800

issn

1096-0945

pii

S0014-4800(10)00087-0

journal_volume

89

pub_type

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