In parallel with the studies of effects of vitamin A deficiency and supplements on populations, there has been an upsurge of investigative effort on functions of vitamin A at the organ and cellular level. Since the balance of public health evidence favours an effect on responses to infection, a logical focus of investigation is the immune system. Research in this area has been reviewed by Ross and Hammerling.18 The topics considered were: integrity of lymphoid organs; gross numbers of different lymphocyte populations; lymphocyte proliferation and functions; circulating antibody concentrations and antibody responses; responses to various types of challenge (eg, by bacterial polysaccharides or lipopolysaccharides, proteins, autologous red cells, viruses, parasitic infections); mucosal immunity; and adjuvant properties of the vitamin. Existing evidence suggests multiple sites of action, but the hierarchy of importance remains to be determined. Vitamin A deficiency does not depress plasma IgM or IgG but secretory immunoglobulins seem more sensitive. Antibody responses to type I antigens, such as bacterial lipopolysaccharides (which are immunogenic even in the absence of functional T cells), are unaffected, whereas antibody responses to type II antigens (eg, bacterial polysaccharides) or proteins or heterologous red cells are clearly subnormal. Subtypes of T cells exhibit differential sensitivity, and natural killer cell numbers and cytotoxic activities were impaired in a rat model. Vitamin A deficiency interferes with responses to measles virus and HIV; it also reduces responses to parasitic infections, but data on mucosal immunity are
sparse.
In parallel with the studies of effects of vitamin A deficiency and supplements on populations, there has been an upsurge of investigative effort on functions of vitamin A at the organ and cellular level. Since the balance of public health evidence favours an effect on responses to infection, a logical focus of investigation is the immune system. Research in this area has been reviewed by Ross and Hammerling.18 The topics considered were: integrity of lymphoid organs; gross numbers of different lymphocyte populations; lymphocyte proliferation and functions; circulating antibody concentrations and antibody responses; responses to various types of challenge (eg, by bacterial polysaccharides or lipopolysaccharides, proteins, autologous red cells, viruses, parasitic infections); mucosal immunity; and adjuvant properties of the vitamin. Existing evidence suggests multiple sites of action, but the hierarchy of importance remains to be determined. Vitamin A deficiency does not depress plasma IgM or IgG but secretory immunoglobulins seem more sensitive. Antibody responses to type I antigens, such as bacterial lipopolysaccharides (which are immunogenic even in the absence of functional T cells), are unaffected, whereas antibody responses to type II antigens (eg, bacterial polysaccharides) or proteins or heterologous red cells are clearly subnormal. Subtypes of T cells exhibit differential sensitivity, and natural killer cell numbers and cytotoxic activities were impaired in a rat model. Vitamin A deficiency interferes with responses to measles virus and HIV; it also reduces responses to parasitic infections, but data on mucosal immunity aresparse.
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