Cutting edge: Critical role for A2A adenosine receptors in the T cell-mediated regulation of colitis

Makoto Naganuma, Elizabeth B. Wiznerowicz, Courtney M. Lappas, Joel Linden, Mark T. Worthington, Peter B. Ernst

Research output: Contribution to journalArticlepeer-review

Abstract

A2A adenosine receptors (A24AR) inhibit inflammation, although the mechanisms through which adenosine exerts its effects remain unclear. Although the transfer of regu-latory Th cells blocks colitis induced by pathogenic CD45RBhigh Th cells, we show that CD45RBlow or CD25+ Th cells from A2AAR-deficient mice do not prevent disease. Moreover, CD45RBhigh Th cells from A2AAR- deficient mice were not suppressed by control CD45RBlow Th cells. A24AR agonists suppressed the production of proinflammatory cytokines by CD45RBhigh and CD45RBlow T cells in association with a loss of mRNA stability. In contrast, anti-inflammatory cytokines, including IL-10 and TGF-β, were minimally affected. Oral administration of the A 24AR agonist ATL313 attenuated disease in mice receiving CD45RB high Th cells. These data suggest that A2AAR play a novel role in the control of T cell-mediated colitis by suppressing the expression of proinflammatory cytokines while sparing anti-inflammatory activity mediated by IL-10 and TGF-β.

Original languageEnglish (US)
Pages (from-to)2765-2769
Number of pages5
JournalJournal of Immunology
Volume177
Issue number5
DOIs
StatePublished - Sep 1 2006

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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