H1 histamine receptor antagonist inhibits constitutive growth of Jurkat T cells and antigen-specific proliferation of ovalbumin-specific murine T cells

Semin Cancer Biol. 2000 Feb;10(1):41-5. doi: 10.1006/scbi.2000.0306.

Abstract

Histamine is produced from histidine by histidine decarboxylase (HDC) in many cells including normal and malignant lymphocytes. We examined the expression of HDC and the effect of histamine receptor antagonists on the proliferation of a human T cell line, Jurkat and on antigen-driven proliferation of lymphocytes from ovalbumin-immunized mice. Our results demonstrate that HDC is inducible in Jurkat cells by anti-CD3. The H1 receptor antagonist triprolidine dose dependently inhibits proliferation of both Jurkat cells and ovalbumin-stimulated murine lymphocytes, while the H2 antagonist ranitidine was ineffective. Alpha-fluoro-methyl-histidine blocking HDC activity did not inhibit the T cell proliferation, suggesting an existing pool of histamine in T cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Histamine / metabolism
  • Histamine H1 Antagonists / pharmacology*
  • Histidine Decarboxylase / metabolism
  • Humans
  • Jurkat Cells / drug effects*
  • Jurkat Cells / enzymology
  • Jurkat Cells / pathology
  • Lymphocyte Activation / drug effects*
  • Mice
  • Ovalbumin / immunology*
  • T-Lymphocytes / immunology*
  • Triprolidine / pharmacology*

Substances

  • Histamine H1 Antagonists
  • Triprolidine
  • Histamine
  • Ovalbumin
  • Histidine Decarboxylase