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 language | English (US) |
|---|---|
| Pages (from-to) | 5637-5645 |
| Number of pages | 9 |
| Journal | Journal of Immunology |
| Volume | 165 |
| Issue number | 10 |
| State | Published - Nov 15 2000 |
| Externally published | Yes |
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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 journal › Article
}
TY - JOUR
T1 - 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
AU - Julia, V.
AU - Mcsorley, Stephen J
AU - Malherbe, L.
AU - Breittmayer, J. P.
AU - Girard-Pipau, F.
AU - Beck, A.
AU - Glaichenhaus, N.
PY - 2000/11/15
Y1 - 2000/11/15
N2 - 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.
AB - 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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M3 - Article
VL - 165
SP - 5637
EP - 5645
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 10
ER -