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Department of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, NC 27858
T cell expression of class II MHC/peptide complexes may be
important for maintenance of peripheral self-tolerance, but mechanisms
underlying the genesis of class II MHC glycoproteins on T cells are not
well resolved. T cell APC (T-APC) used herein were transformed
IL-2-dependent clones that constitutively synthesized class II MHC
glycoproteins. When pulsed with myelin basic protein (MBP) and injected
into Lewis rats, these T-APC reduced the severity of experimental
autoimmune encephalomyelitis, whereas unpulsed T-APC were without
activity. Normal MBP-reactive clones cultured without APC did not
express class II MHC even when activated with mitogens and exposed to
IFN-
. However, during a 4-h culture with T-APC or macrophage APC,
recognition of MBP or mitogenic activation of responder T cells
elicited high levels of I-A and I-E expression on responders.
Acquisition of class II MHC glycoproteins by responders was resistant
to the protein synthesis inhibitor cycloheximide, coincided with
transfer of a PKH26 lipophilic dye from APC to responders, and resulted
in the expression of syngeneic and allogeneic MHC glycoproteins on
responders. Unlike rested I-A- T cell clones, rat thymic
and splenic T cells expressed readily detectable levels of class II MHC
glycoproteins. When preactivated with mitogens, naive T cells acquired
APC-derived MHC class II molecules and other membrane-associated
proteins when cultured with xenogeneic APC in the absence of Ag. In
conclusion, this study provides evidence that APC donate membrane-bound
peptide/MHC complexes to Ag-specific T cell responders by a mechanism
associated with the induction of tolerance.
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