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Helper-independent CD8+ cytotoxic T lymphocytes express IL-1 receptors and require IL-1 for secretion of IL-2.

Abstract
The purpose of this study was to examine the role of IL-1 on the activation of CD8+/CD4- class I-restricted helper cell-independent cytolytic T cell (HITc) clones known to produce IL-2 and proliferate in vitro after Ag stimulation with a Friend retrovirus-induced leukemia (FBL). The functional role of IL-1 in Ag-specific proliferation and IL-2 secretion was assessed by stimulating the T cell clones with FBL either in the presence or absence of macrophages (M phi), rIL-1, or rIL-2. Resting cloned HITc cells, purified from residual accessory cells, failed to proliferate in response to FBL alone, but proliferated in response to FBL plus M phi, rIL-1 or rIL-2. Stimulation with FBL alone in the absence of M phi or IL-1 was sufficient for induction of IL-2R expression, and rendered cells responsive to IL-2, but M phi or IL-1 were also required to induce production of IL-2. The activity of IL-1 was further examined by measuring the binding of [125I]rIL-1 alpha, which demonstrated that resting cloned HITc cells expressed IL-1R that increased in number after activation with Ag. This expression of IL-1R and requirement for IL-1 by CD8+ HITc was surprising because previous studies examining T cell populations after mitogen stimulation have not detected IL-1R on the CD8+ population. Therefore, the role of IL-1 in the activation of CD8+ CTL that do not secrete IL-2 after activation was assessed. By contrast to HITc, CD8+ CTL required exogenous IL-2 to proliferate in vitro and did not express IL-1R. These data demonstrate that the subset of CD8+ T cells responsible for IL-2 production express IL-1R and that triggering this receptor with IL-1 after Ag stimulation results in the production of IL-2 and subsequent proliferation.
AuthorsJ P Klarnet, D E Kern, S K Dower, L A Matis, M A Cheever, P D Greenberg
JournalJournal of immunology (Baltimore, Md. : 1950) (J Immunol) Vol. 142 Issue 7 Pg. 2187-91 (Apr 01 1989) ISSN: 0022-1767 [Print] United States
PMID2466890 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Antigens, Differentiation, T-Lymphocyte
  • Epitopes
  • Interleukin-1
  • Interleukin-2
  • Receptors, Immunologic
  • Receptors, Interleukin-1
  • Recombinant Proteins
Topics
  • Animals
  • Antigens, Differentiation, T-Lymphocyte
  • Clone Cells (immunology, metabolism)
  • Epitopes
  • Female
  • Interleukin-1 (metabolism, physiology)
  • Interleukin-2 (biosynthesis)
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred C57BL
  • Phenotype
  • Receptors, Immunologic (biosynthesis, metabolism)
  • Receptors, Interleukin-1
  • Recombinant Proteins (metabolism)
  • T-Lymphocytes (classification, physiology)
  • T-Lymphocytes, Helper-Inducer (immunology)

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