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Effects of anti-Lyt-2 and anti-L3T4 monoclonal antibodies on the function of cytotoxic T lymphocyte/helper T lymphocyte hybrid T cell clones

Academic Article
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Overview

authors

  • Havran, Wendy
  • Fitch, F. W.

publication date

  • 1988

journal

  • Journal of Immunology  Journal

abstract

  • CTL/HTL hybrid clones provide a unique system that allows detailed analysis of the role of Lyt-2, L3T4, and other structures involved in T cell functions. We have demonstrated previously that the fusion of cloned murine CTL and helper T lymphocytes with defined specificity generated hybrid cells that expressed both Lyt-2 and L3T4 as well as two TCR. Data obtained with these hybrid clones demonstrated that cytolysis is closely linked to the CTL TCR. We have analyzed the effects of anti-Lyt-2 and anti-L3T4 as well as anti-TCR mAb on cytolysis, proliferation, and lymphokine release by a number of hybrid clones. We found that anti-Lyt-2 and anti-L3T4 mAb were able to inhibit both proliferation and lymphokine release by the hybrid clones in response to stimulation of either the CTL or helper T lymphocyte parent TCR. In contrast, only anti-Lyt-2 and anti-CTL TCR mAb were able to block cytolysis of target cells bearing the Ag recognized by the CTL TCR. These results provide further evidence that cytolysis is closely linked to the CTL TCR and that Lyt-2 and L3T4 have more than a passive role as accessory molecules on the surface of T lymphocytes.

subject areas

  • Animals
  • Antibodies, Monoclonal
  • Antigens, Differentiation, T-Lymphocyte
  • Antigens, Ly
  • Binding, Competitive
  • Clone Cells
  • Cytotoxicity, Immunologic
  • Epitopes
  • Hybridomas
  • Immunosuppressive Agents
  • Lymphocyte Activation
  • Lymphokines
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Inbred CBA
  • Mice, Inbred DBA
  • Receptors, Antigen, T-Cell
  • T-Lymphocytes, Cytotoxic
  • T-Lymphocytes, Helper-Inducer
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 2459190
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Additional Document Info

start page

  • 1808

end page

  • 1812

volume

  • 141

issue

  • 6

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