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CD4+ T Cell Responses to Simian Immunodeficiency Virus

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Simian Immunodeficiency Virus

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 188))

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Abstract

T cells have classically been divided into two populations on the basis of their surface phenotype, MHC restriction and function. CD8+ T cells recognize endogenous antigen in association with MHC class I molecules and display cytotoxic activity against infected or peptide-pulsed target cells. Although these cytotoxic T lymphocytes (CTL) have usually been described following infection with viruses or intracellular bacteria, they can also be induced with soluble peptides or proteins, especially when the antigen is associated with lipids, which appears to facilitate their transport from intracellular vesicles into the cytoplasm. In contrast, a second population of T cells that express the CD4+ molecule are readily induced with soluble proteins and recognise exogenous processsed antigen in association with MHC class II molecules. Although these cells ahve traditionally been called T helper (Th) cells, in that they provide helper function for B cell production of antibody, recent evidence suggests that they play a more diverse role including the regulation and effector function of cellular immune responses against foreign pathogens. Studies with murine T cell clones and, more recently, human T cell clones have shown that CD4+ T cells can be further divided into two subpopulations on the basis of their cytokine production and function (Mossmann et al. 1986; Romagnani 1991). One subpopulation, termed Th1 cells, secrete interleukin (IL) 2, interferon (IFN) γ and lymphotoxin and, as CD8+ T cells, display cytotoxic activity against antigen-pulsed target cells.

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© 1994 Springer-Verlag Berlin Heidelberg

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Mills, K.H.G., Jones, W.C. (1994). CD4+ T Cell Responses to Simian Immunodeficiency Virus. In: Letvin, N.L., Desrosiers, R.C. (eds) Simian Immunodeficiency Virus. Current Topics in Microbiology and Immunology, vol 188. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-78536-8_9

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  • DOI: https://doi.org/10.1007/978-3-642-78536-8_9

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-78538-2

  • Online ISBN: 978-3-642-78536-8

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