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J. Exp. Med.,
Volume 188, Number 10, November 16, 1998 1883-1894
By
From the * Division of Molecular Pathogenesis, Skirball Institute of Biomolecular Medicine, and the
Department of Pathology, and the The development of T cell-mediated autoimmune diseases hinges on the balance between effector and regulatory mechanisms. Using two transgenic mouse lines expressing identical myelin basic protein (MBP)-specific T cell receptor (TCR) genes, we have previously shown that
mice bearing exclusively MBP-specific T cells (designated T/R Sackler Institute of Graduate Biomedical Sciences, New York
University Medical Center, New York 10016
) spontaneously develop experimental autoimmune encephalomyelitis (EAE), whereas mice bearing MBP-specific T cells
as well as other lymphocytes (designated T/R+) did not. Here we demonstrate that T/R
mice can be protected from EAE by the early transfer of total splenocytes or purified CD4+ T
cells from normal donors. Moreover, whereas T/R+ mice crossed with B cell-deficient, 
/
T
cell-deficient, or major histocompatibility complex class I-deficient mice did not develop EAE
spontaneously, T/R+ mice crossed with TCR-
and -
knockout mice developed EAE with the same incidence and severity as T/R mice. In addition, MBP-specific transgenic mice that
lack only endogenous TCR- chains developed EAE with high incidence but reduced severity. Surprisingly, two-thirds of MBP-specific transgenic mice lacking only endogenous TCR-
chains also developed EAE, suggesting that in T/R+ mice, cells with high protective activity
escape TCR- chain allelic exclusion. Our study identifies CD4+ T cells bearing endogenous
and TCR chains as the lymphocytes that prevent spontaneous EAE in T/R+ mice.
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