GABA(A) receptors mediate inhibition of T cell responses

J Tian, C Chau, T G Hales, D L Kaufman

Research output: Contribution to journalArticlepeer-review

151 Citations (Scopus)


We describe the presence of functional GABA(A) receptors on T cells. GABA inhibited anti-CD3 and antigen-specific T cell proliferation in vitro in a dose-dependent manner that was 1) mimicked by the GABA(A) receptor agonist muscimol (but not the GABA(B) receptor agonist baclofen), 2) blocked by GABA(A) receptor antagonists and a GABA(A) receptor Cl- channel blocker (picrotoxin) and 3) enhanced by pentobarbital. These data suggest that GABA(A) receptors mediate this immune inhibition and that these receptors can be modulated in a similar fashion to their neuronal counterparts. Finally, GABA inhibited DTH responses in vivo. Thus, pharmacological modulation of GABA(A) receptors may provide new approaches to modulate T cell responses in inflammation and autoimmune disease.

Original languageEnglish
Pages (from-to)21-8
Number of pages8
JournalJournal of Neuroimmunology
Issue number1
Publication statusPublished - 1 Apr 1999


  • Amidines/pharmacology
  • Animals
  • Autocrine Communication/immunology
  • Bicuculline/pharmacology
  • CD3 Complex/analysis
  • Cell Division/immunology
  • Enzyme Inhibitors/pharmacology
  • Female
  • GABA Agonists/pharmacology
  • GABA Antagonists/pharmacology
  • GABA Modulators/pharmacology
  • Hypersensitivity, Delayed
  • Immunosuppression
  • Interleukin-2/biosynthesis
  • Lymphocyte Activation/drug effects
  • Male
  • Mice
  • Mice, Inbred NOD
  • Muscimol/pharmacology
  • Pentobarbital/pharmacology
  • Picrotoxin/pharmacology
  • Receptors, GABA-A/immunology
  • Receptors, GABA-B/immunology
  • Signal Transduction/immunology
  • T-Lymphocytes/chemistry
  • Vigabatrin
  • gamma-Aminobutyric Acid/analogs & derivatives


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