Assessment of lymphocyte function during vitamin A deficiency.
Two variables of immune status were measured in vitamin A-deficient (A-), vitamin A-sufficient pair-fed (A + PF), and healthy control (A+) rats to examine the mechanisms of immune regulation by vitamin A. Parallel samples were run in bovine fetal serum (BFS)-containing medium and serum-free medium to control BFS-origin vitamin A in the cultures. Splenocytes derived from A- rats showed significantly depressed blastogenic response to all lectins tested in both mediums when compared with responses of A + PF and A+ rats. The splenocyte blastogenic response of A + PF rats was significantly lower than that of A+ (control) rats only when cultured in BFS medium and stimulated by lentil lectin, lipopolysaccharide, or concanavalin A mitogens. Thymic lymphocyte blastogenic transformation assays were equivocal. Splenic immunosuppression could not be linked to significant reductions in surface glycoprotein receptor availability, since splenocytes of A- rats, as well as thymocytes, were capable of binding fluorescein isothiocyanate-conjugated lectins in the same capacity as splenocytes of A+ and A + PF rats. The combination of depressed cellular function and adequate lectin binding to viable cells implies that the regulation of immunohomeostasis by vitamin A was achieved through intracellular mechanisms, possibly selective genomic expression.
D000818:Animals; D002478:Cells, Cultured; D008099:Liver / Q000032:analysis; D008213:Lymphocyte Activation / Q000187:drug effects; D008214:Lymphocytes / Q000187:drug effects / Q000276:immunology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011975:Receptors, Mitogen / Q000032:analysis; D012016:Reference Values; D013154:Spleen / Q000473:pathology; D013950:Thymus Gland / Q000473:pathology; D014801:Vitamin A / Q000032:analysis / Q000494:pharmacology; D014802:Vitamin A Deficiency / Q000276:immunology* / Q000473:pathology
D011975:Receptors, Mitogen; D014801:Vitamin A