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Department of Cancer Immunology and AIDS, Dana Farber Cancer Institute, Department of Pathology, Harvard Medical School, Boston, MA 02115
We have investigated the role of MHC class I products and CD8 T cells in regulating Ab responses using ß2-microglobulin deficient (ß2m-/-) mice. ß2m-/- mice produced stronger IgM and IgG responses than did control ß2m+/+ mice to both cellular and viral Ags. These Ab responses could be suppressed by infusion of activated B cells from ß2m+/+ mice. Further investigation showed that the ß2m-associated molecule on activated B cells that induced CD8 suppression was Qa-1 and that the Th2 component of CD4 cells was most affected by CD8-suppressive activity. Our findings suggest a novel pathway of Th inhibition in which B cell presentation of Qa-1-associated peptides stimulates CD8 suppressive activity.
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