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T cell proliferation in vivo is presumed to reflect a T cell receptor (TCR)-mediated polyclonal response directed to various environmental antigens. However, the massive proliferation of T cells seen in viral infections is suggestive of a bystander reaction driven by cytokines instead of the TCR. In mice, T cell proliferation in viral infections preferentially affected the CD44hi subset of CD8+ cells and was mimicked by injection of polyinosinic-polycytidylic acid [poly(I:C)], an inducer of type I interferon (IFN I), and also by purified IFN I; such proliferation was not associated with up-regulation of CD69 or CD25 expression, which implies that TCR signaling was not involved. IFN I [poly(I:C)]-stimulated CD8+ cells survived for prolonged periods in vivo and displayed the same phenotype as did long-lived antigen-specific CD8+ cells. IFN I also potentiated the clonal expansion and survival of CD8+ cells responding to specific antigen. Production of IFN I may thus play an important role in the generation and maintenance of specific memory.

Type

Journal article

Journal

Science

Publication Date

28/06/1996

Volume

272

Pages

1947 - 1950

Keywords

Animals, Antigens, CD, Antigens, Differentiation, T-Lymphocyte, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Cell Division, Cell Survival, Hyaluronan Receptors, Immunologic Memory, Immunophenotyping, Interferon Type I, Lectins, C-Type, Lymphocyte Activation, Lymphocytic Choriomeningitis, Lymphocytic choriomeningitis virus, Mice, Mice, Inbred C57BL, Mice, Transgenic, Poly I-C, Receptors, Antigen, T-Cell, Receptors, Interleukin-2