Author
Stephensen, Charles | |
JIANG, XIAOWEN - UNIV OF CALIF DAVIS | |
FREYTAG, TAMMY - UNIV OF CALIF DAVIS |
Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 7/1/2004 Publication Date: 10/1/2004 Citation: Stephensen, C.B., Jiang, X., Freytag, T. 2004. Vitamin a deficiency increases the in vivo development of il-10-positive th2 and decreases development of th1 cells in mice. Journal of Nutrition. 134:2660-2666. Interpretive Summary: Technical Abstract: Vitamin A deficiency impairs both Th1- and Th2-mediated immune responses. Multiple mechanisms are involved but the hypothesis that deficiency affects development of Th1/Th2 memory cell phenotype, has not been directly tested in vivo. To do so, lymphocytes from DO11.10 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). Two to five weeks later the transferred OVA323-339-specific T-cells were identified from draining lymph nodes with the CRclonotypic antibody KJ1-26 and their Th1/Th2 phenotype was characterized by intracellular cytokine staining following in vitro stimulation with phorbol myristate acetate and ionomycin. The percentage of CD4+KJ1-26+ cells positive for IL-10 was two-fold greater in vitamin A-deficient mice (3.49 +/-0.41%; mean standard error) than in control mice (1.74 +/-0.37%). No difference was seen for IL-4. In addition, the percentages of CD4+KJ1-26+ cells from vitamin A-deficient mice that were positive for IFN-10 (8.8 +/-0.73%) and IL-2 (39.5 +/-3.1%) were both lower than the percentages seen 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 Treg cells and diminishes the development of Th1 memory cells. This work was supported by USDA NRI grant # 97-35200-4229, USDA CRIS Project # 5306-51530-006-00D and NIH grant # 1 R01 AI 0863. |