The effects of vitamin A deficiency on the immune system in a murine model of systemic lupus erythematosus
Liao, C. Hua
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Permalink
https://hdl.handle.net/2142/20750
Description
Title
The effects of vitamin A deficiency on the immune system in a murine model of systemic lupus erythematosus
Author(s)
Liao, C. Hua
Issue Date
1993
Doctoral Committee Chair(s)
Klein, Barbara P.
Department of Study
Human and Community Development
Discipline
Human and Community Development
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Cell
Health Sciences, Nutrition
Health Sciences, Immunology
Language
eng
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.
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