Vitamin A deficiency increases the in vivo development of IL-10-positive Th2 cells and decreases development of Th1 cells in mice.
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 (OVA(323-339)). After 2-5 wk, the transferred OVA(323-339)-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)-gamma (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.
Stephensen
Charles B
CB
U.S. Department of Agriculture, Western Human Nutrition Research Center at the University of California, Davis, and Nutrition Department, University of California, Davis, CA 95616, USA. cstephensen@ucdavis.edu
Jiang
Xiaowen
X
Freytag
Tammy
T
D000818:Animals; D000831:Animals, Newborn; D005260:Female; D007156:Immunologic Memory / Q000276:immunology / Q000502:physiology; D016753:Interleukin-10 / Q000096:biosynthesis*; D008198:Lymph Nodes / Q000276:immunology* / Q000378:metabolism; D008431:Maternal-Fetal Exchange; D051379:Mice; D010047:Ovalbumin / Q000096:biosynthesis* / Q000276:immunology; D010446:Peptide Fragments / Q000096:biosynthesis* / Q000276:immunology; D011247:Pregnancy; D013388:Succinimides; D018417:Th1 Cells / Q000276:immunology* / Q000502:physiology; D018418:Th2 Cells / Q000276:immunology* / Q000502:physiology; D014801:Vitamin A / Q000097:blood; D014802:Vitamin A Deficiency / Q000276:immunology* / Q000378:metabolism
C111390:OVA 323-339; D010446:Peptide Fragments; D013388:Succinimides; D014801:Vitamin A; D016753:Interleukin-10; C037891:3,5-dibromophenylsuccinic acid N-methylimide; D010047:Ovalbumin