Priming by microbial antigens from the intestinal flora determines the ability of CD4+ T cells to rapidly secrete IL-4 in BALB/c mice infected with Leishmania major

V. Julia, Stephen J Mcsorley, L. Malherbe, J. P. Breittmayer, F. Girard-Pipau, A. Beck, N. Glaichenhaus

Research output: Contribution to journalArticle

51 Scopus citations

Abstract

Infection of BALB/c mice with Leishmania major results in the rapid accumulation of IL-4 transcripts within CD4+ T cells that react to the parasite Leishmania homologue of mammalian RACK1 (LACK) Ag. Because memory/effector cells secrete IL-4 more rapidly than naive cells, we sought to analyze the phenotype of these lymphocytes before infection. Indeed, a fraction of LACK-specific CD4+ T cells expressed a typical CD62 ligand(low)CD44(high)CD45RB(low) phenotype in uninfected mice. LACK-specific T cells were primed in gut-associated lymphoid tissues by cross-reactive microbial Ags as demonstrated by their reactivity with bacterial extracts and by the ability of APCs from the mesenteric LN of BALB/c mice to induce their proliferation. Also, mice in which the digestive tract has been decontaminated exhibited a reduced proportion of LACK-specific T cells expressing a memory/effector phenotype and did not exhibit the early accumulation of IL-4 transcripts induced by L. major. Thus, LACK-specific T cells represent a subset of CD4+ T cells which have acquired the ability to rapidly secrete IL-4 as the result of their priming by cross-reactive microbial Ags. Tracking the fate of these cells may provide information about the regulation of cell-mediated immune responses to gut Ags in physiological and pathological situations.

Original languageEnglish (US)
Pages (from-to)5637-5645
Number of pages9
JournalJournal of Immunology
Volume165
Issue number10
StatePublished - Nov 15 2000
Externally publishedYes

ASJC Scopus subject areas

  • Immunology

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