Vitamin A deficiency increases the in vivo development of IL-10-positive Th2 cells and decreases development of Th1 cells in mice

Charles B. Stephensen, Xiaowen Jiang, Tammy Freytag

Research output: Contribution to journalArticle

65 Citations (Scopus)

Abstract

Vitamin A deficiency impairs both T helper type 1 (Th1)- and type 2 (Th2)-mediated immune responses, although Th2 responses seem to be principally affected. Multiple mechanisms are involved in this immune suppression, but the hypothesis that deficiency affects development of Th1/Th2 memory cell phenotype has not been tested directly in vivo. To do so, lymphocytes from DO11.10 T cell receptor (TCR)-transgenic mice were transferred to vitamin A-deficient or control BALB/c recipients. Recipients were then immunized with the cognate peptide antigen for the TCR-transgenic DO11.10 T cells (OVA323_339). After 2-5 wk, the transferred OVA323_339-specific T cells were identified from draining lymph nodes with the TCR-clonotypic antibody KJ1-26, and their Th1/Th2 phenotype was characterized by intracellular cytokine staining after in vitro stimulation with phorbol myristate acetate and ionomycin. The percentage of CD4+KJ1-26+ cells positive for IL-10 was 100% greater in vitamin A-deficient mice (3.49 ± 0.41%; mean ± SE) than in control mice (1.74 ± 0.37%). IL-4 did not differ between groups. In addition, the percentages of CD4+KJ1-26+ cells from vitamin A-deficient mice that were positive for interferon (IFN)-γ (8.8 ± 0.73%) and interleukin (IL)-2 (39.5 ± 3.1%) were both lower than the percentages in control mice (11.4 ± 0.67 and 47.0 ± 2.8%, respectively). Thus vitamin A deficiency, at the time of initial antigen exposure, enhances the development of IL-10-producing Th2 or T regulatory cells and diminishes the development of Th1 memory cells.

Original languageEnglish (US)
Pages (from-to)2660-2666
Number of pages7
JournalJournal of Nutrition
Volume134
Issue number10
StatePublished - Oct 2004
Externally publishedYes

Fingerprint

Vitamin A Deficiency
Th2 Cells
Th1 Cells
vitamin A deficiency
interleukin-10
Interleukin-10
T-lymphocytes
T-Cell Antigen Receptor
Vitamin A
mice
vitamin A
receptors
cells
Peptide T
T-Lymphocytes
Phenotype
Antigens
Ionomycin
genetically modified organisms
antigens

Keywords

  • Immunomodulators
  • Rodent
  • Th1/Th2
  • Transgenic/knockout
  • Vitamin A deficiency

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

Vitamin A deficiency increases the in vivo development of IL-10-positive Th2 cells and decreases development of Th1 cells in mice. / Stephensen, Charles B.; Jiang, Xiaowen; Freytag, Tammy.

In: Journal of Nutrition, Vol. 134, No. 10, 10.2004, p. 2660-2666.

Research output: Contribution to journalArticle

Stephensen, Charles B. ; Jiang, Xiaowen ; Freytag, Tammy. / Vitamin A deficiency increases the in vivo development of IL-10-positive Th2 cells and decreases development of Th1 cells in mice. In: Journal of Nutrition. 2004 ; Vol. 134, No. 10. pp. 2660-2666.
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abstract = "Vitamin A deficiency impairs both T helper type 1 (Th1)- and type 2 (Th2)-mediated immune responses, although Th2 responses seem to be principally affected. Multiple mechanisms are involved in this immune suppression, but the hypothesis that deficiency affects development of Th1/Th2 memory cell phenotype has not been tested directly in vivo. To do so, lymphocytes from DO11.10 T cell receptor (TCR)-transgenic mice were transferred to vitamin A-deficient or control BALB/c recipients. Recipients were then immunized with the cognate peptide antigen for the TCR-transgenic DO11.10 T cells (OVA323_339). After 2-5 wk, the transferred OVA323_339-specific T cells were identified from draining lymph nodes with the TCR-clonotypic antibody KJ1-26, and their Th1/Th2 phenotype was characterized by intracellular cytokine staining after in vitro stimulation with phorbol myristate acetate and ionomycin. The percentage of CD4+KJ1-26+ cells positive for IL-10 was 100{\%} greater in vitamin A-deficient mice (3.49 ± 0.41{\%}; mean ± SE) than in control mice (1.74 ± 0.37{\%}). IL-4 did not differ between groups. In addition, the percentages of CD4+KJ1-26+ cells from vitamin A-deficient mice that were positive for interferon (IFN)-γ (8.8 ± 0.73{\%}) and interleukin (IL)-2 (39.5 ± 3.1{\%}) were both lower than the percentages in control mice (11.4 ± 0.67 and 47.0 ± 2.8{\%}, respectively). Thus vitamin A deficiency, at the time of initial antigen exposure, enhances the development of IL-10-producing Th2 or T regulatory cells and diminishes the development of Th1 memory cells.",
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N2 - Vitamin A deficiency impairs both T helper type 1 (Th1)- and type 2 (Th2)-mediated immune responses, although Th2 responses seem to be principally affected. Multiple mechanisms are involved in this immune suppression, but the hypothesis that deficiency affects development of Th1/Th2 memory cell phenotype has not been tested directly in vivo. To do so, lymphocytes from DO11.10 T cell receptor (TCR)-transgenic mice were transferred to vitamin A-deficient or control BALB/c recipients. Recipients were then immunized with the cognate peptide antigen for the TCR-transgenic DO11.10 T cells (OVA323_339). After 2-5 wk, the transferred OVA323_339-specific T cells were identified from draining lymph nodes with the TCR-clonotypic antibody KJ1-26, and their Th1/Th2 phenotype was characterized by intracellular cytokine staining after in vitro stimulation with phorbol myristate acetate and ionomycin. The percentage of CD4+KJ1-26+ cells positive for IL-10 was 100% greater in vitamin A-deficient mice (3.49 ± 0.41%; mean ± SE) than in control mice (1.74 ± 0.37%). IL-4 did not differ between groups. In addition, the percentages of CD4+KJ1-26+ cells from vitamin A-deficient mice that were positive for interferon (IFN)-γ (8.8 ± 0.73%) and interleukin (IL)-2 (39.5 ± 3.1%) were both lower than the percentages in control mice (11.4 ± 0.67 and 47.0 ± 2.8%, respectively). Thus vitamin A deficiency, at the time of initial antigen exposure, enhances the development of IL-10-producing Th2 or T regulatory cells and diminishes the development of Th1 memory cells.

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