PubMed:9973402 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/9973402","sourcedb":"PubMed","sourceid":"9973402","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/9973402","text":"Evidence for repression of IL-2 gene activation in anergic T cells.\nThe induction of clonal anergy in a T cell inhibits IL-2 secretion because of the development of a proximal signal transduction defect. Fusion of anergic murine T cells to human Jurkat T leukemia cells and formation of heterokaryons failed to result in a complementation of this signaling defect and restoration of murine IL-2 mRNA inducibility. Instead, signal transduction to the human IL-2 gene became disrupted. Heterokaryons formed by the fusion of anergic murine T cells to normal murine T cells also failed to accumulate intracellular IL-2 protein in response to stimulation either with the combination of CD3 and CD28 mAbs or with ionomycin plus a protein kinase C-activating phorbol ester. The results argue against a loss-of-function signaling defect as the sole basis for clonal anergy induction and document the presence of a dominant-acting repressor molecule that inhibits signal transduction to the IL-2 gene within viable anergic T 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