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,
Departments of
*
Pediatrics,
Medicine, and
Pathology, Washington University School of Medicine, St. Louis, MO 63110
T cell unresponsiveness to Ag stimulation can be induced by several
means. The precise mechanism by which this process occurs remains
poorly understood. Preincubating T cells with either EDCI-fixed APC or
ionomycin is a proven means of inducing T cell anergy with reduced IL-2
production in response to Ag stimulation. Using T cells from mice
expressing the TCR transgene DO11.10, which is specific for a peptide
(323–339) derived from hen egg OVA, we demonstrate that naive cells
obtained directly from the host are resistant to the anergy induction
by either fixed APC or ionomycin. TCR transgenic mice also deficient in
the recombination-activating gene-2 (RAG-2-/-),
preventing the formation of T cells with endogenous TCRs, were
immunized with OVA, and in vivo activated T cells with low expression
of CD62 were isolated. These primed cells possess the same sensitivity
to ionomycin-induced anergy as in vitro activated cell lines. This
unresponsive state most profoundly affects Ag-induced IL-2 production,
with IFN-
and IL-3 affected to a lesser degree and no effect
observed on IL-4 production. Thus, T cells in vivo can be distinguished
phenotypically by their susceptibility to anergic stimuli. Anergy so
induced affects selected T cell functions.
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