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

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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

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Leishmania major
Aptitude
Interleukin-4
T-Lymphocytes
Antigens
Phenotype
Cell Tracking
Leishmania
T-Lymphocyte Subsets
Lymphoid Tissue
Infection
Gastrointestinal Tract
Parasites
Gastrointestinal Microbiome
Lymphocytes
Ligands

ASJC Scopus subject areas

  • Immunology

Cite this

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

In: Journal of Immunology, Vol. 165, No. 10, 15.11.2000, p. 5637-5645.

Research output: Contribution to journalArticle

Julia, V. ; Mcsorley, Stephen J ; Malherbe, L. ; Breittmayer, J. P. ; Girard-Pipau, F. ; Beck, A. ; Glaichenhaus, N. / 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. In: Journal of Immunology. 2000 ; Vol. 165, No. 10. pp. 5637-5645.
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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.",
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