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,
*
Veterans Affairs Medical Center, Memphis, TN 38104; and Departments of
Medicine,
Pathology, and
Pediatrics, University of Tennessee Health Sciences Center, Memphis, TN 38163
To study the phenotypic and functional changes in naive type II
collagen (CII)-specific autoimmune T cells following a tolerogenic
signal, a TCR-transgenic (Tg) mouse model of collagen-induced arthritis
was developed. These Tg mice express an I-Aq-restricted CII
(260–267)-specific TCR that confers severe accelerated autoimmune
arthritis following immunization with CII. Despite the fact that >90%
of the 
T cells express the Tg, these mice can be rendered
completely tolerant to the induction of arthritis by i.v.
administration of 200 µg of CII. As early as 24 h after CII
administration, CII-specific T cells demonstrated a decreased ability
to proliferate in response to the CII immunodominant peptide and
phenotypically altered the expression of L-selectin to
CD62Llow and of phagocytic glycoprotein-1 to
CD44high, expression levels consistent with the phenotype
of memory T cells. In addition, they up-regulated the expression of the
activation markers CD71 and CD69. Functionally, following tolerogenic
stimulation, the CII-specific T cells produced similar levels of IL-2
in comparison to controls when challenged with CII peptide, however, by
48 h after exposure to tolerogen, IL-2 production dropped and was
replaced by high levels of IL-10 and IL-4. Based on their production of
Th2 cytokines, these data suggest that T regulatory cells expressing
activation and memory markers are induced by the tolerogen and may
exert their influence via cytokines to protect the animals from the
induction of arthritis.
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