An important role of prostanoid receptor EP2 in host resistance to mycobacterium tuberculosis infection in mice

Vandana Kaul, Debapriya Bhattacharya, Yogesh Singh, Luc Van Kaer, Marc Peters-Golden, William R. Bishai, Gobardhan Das

Research output: Contribution to journalReview article

Abstract

Mycobacterium tuberculosis, the causative agent of tuberculosis, resides and replicates within susceptible hosts by inhibiting host antimicrobial mechanisms. Prostaglandin E2 (PGE2), produced by M. tuberculosis-infected macrophages, exerts a variety of immunomodulatory functions via 4 receptors (EP1-EP4), each mediating distinct PGE2 functions. Here, we show that M. tuberculosis infection selectively upregulates EP2 messenger RNA expression in CD4+ T cells. We found that EP2 deficiency in mice increases susceptibility to M. tuberculosis infection, which correlated with reduced antigen-specific T-cell responses and increased levels of CD4+CD25+Foxp3+ T-regulatory cells. These findings have revealed an important role for EP2 in host immune defense against tuberculosis. As a G protein-coupled receptor, EP2 could serve as a target for immunotherapy of tuberculosis.

Original languageEnglish (US)
Pages (from-to)1816-1825
Number of pages10
JournalJournal of Infectious Diseases
Volume206
Issue number12
DOIs
StatePublished - Dec 15 2012

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

Fingerprint Dive into the research topics of 'An important role of prostanoid receptor EP2 in host resistance to mycobacterium tuberculosis infection in mice'. Together they form a unique fingerprint.

  • Cite this