TIR domain-containing adapter-inducing beta interferon (TRIF) mediates immunological memory against bacterial pathogens

Saravana Kanagavelu, Claudia Flores, J. M. Termini, Laura Romero, Reldy Riveron, Jose Ruiz, Moshe Arditi, Kurt Schesser, Masayuki Fukata

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

Induction of adaptive immunity leads to the establishment of immunological memory; however, how innate immunity regulates memory T cell function remains obscure. Here we show a previously undefined mechanism in which innate and adaptive immunity are linked by TIR domain-containing adapter-inducing beta interferon (TRIF) during establishment and reactivation of memory T cells against Gram-negative enteropathogens. Absence of TRIF in macrophages (Mπs) but not dendritic cells led to a predominant generation of CD4+ central memory T cells that express IL-17 during enteric bacterial infection in mice. TRIFdependent type I interferon (IFN) signaling in T cells was essential to Th1 lineage differentiation and reactivation of memory T cells. TRIF activated memory T cells to facilitate local neutrophil influx and enhance bacterial elimination. These results highlight the importance of TRIF as a mediator of the innate and adaptive immune interactions in achieving the protective properties of memory immunity against Gram-negative bacteria and suggest TRIF as a potential therapeutic target.

Original languageEnglish (US)
Pages (from-to)4404-4415
Number of pages12
JournalInfection and immunity
Volume83
Issue number11
DOIs
StatePublished - 2015

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

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