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Title:The effects of vitamin A deficiency on the immune system in a murine model of systemic lupus erythematosus
Author(s):Liao, C. Hua
Doctoral Committee Chair(s):Klein, Barbara P.
Department / Program:Human and Community Development
Discipline:Human and Community Development
Degree Granting Institution:University of Illinois at Urbana-Champaign
Subject(s):Biology, Cell
Health Sciences, Nutrition
Health Sciences, Immunology
Abstract:The objectives of the present study were to investigate the effects of vitamin A deficiency on the onset and progression of systemic lupus erythematosus (SLE), using the murine model, MRL/MPJ-lpr/lpr (MRL/l) mice in comparison with MRL/MP-+/+ (+/+) mice, and to postulate a possible mechanism. In Study I, sixty weanling female four week old MRL/l mice were randomly assigned to either the vitamin A-deficient (A-), A-sufficient (A+), and A-sufficient diet/feed restricted (DR) groups. In Study II fifty-eight same-age and -sex MRL/l mice were randomly assigned to either the A$-$ or A+ groups, while twenty-four +/+ mice, of the same sex and age range as MRL/l, were assigned to the normal control group (+/+ group). The results of both studies showed that vitamin A deficiency had a significant effect on preventing the MRL/l mice body weight loss due to the progression of SLE. Vitamin A deficiency also tended to suppress the abnormal enlargement of the thymus and spleen due to massive proliferation of abnormal T cells in MRL/l mice. The results of in vitro splenocyte proliferation tests indicate that vitamin A deficiency decreased the proportion of abnormal T and hypersecreation B cells so that the normal T and B cell ratio increased and was closer to the +/+ group in MRL/l mice. The results from Study II strongly suggested that the above beneficial effects of vitamin A deficiency were related to an increased expression of interleukin-2 (IL-2) receptor on the surface of the MRL/l mouse splenocytes, which resulted in an increased proliferation of normal T and B cells. To summarize, vitamin A deficiency decreases the overall progression of SLE in MRL/l mice. The mechanism includes an increased activity of suppressor T cells and an increased expression of IL-2 receptors on the surface of the splenocytes.
Issue Date:1993
Rights Information:Copyright 1993 Liao, C. Hua
Date Available in IDEALS:2011-05-07
Identifier in Online Catalog:AAI9314904
OCLC Identifier:(UMI)AAI9314904

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