Antibody responses

The hallmark of vitamin A deficiency is an impaired capacity to generate an antibody response to T-cell-dependent antigens (Smith and Hayes, 1987; Semba et al., 1992, 1994; Wiedermann et al., 1993a, b) and T-cell-independent type 2 antigens, such as pneumococcal polysaccharide (Pasatiempo et al., 1989). Antibody responses are involved in protective immunity to many types of infections and are the main basis for immunological protection for most types of vaccines. Depressed antibody responses to tetanus toxoid have been observed in vitamin A-deficient children (Semba et al., 1992) and animals (Lavasa et al., 1988; Pasatiempo et al., 1990). Vitamin A deficiency appears to impair the generation of primary antibody responses to tetanus toxoid, but, if animals are replete with vitamin A prior to a second immunization, the secondary antibody responses to tetanus toxoid are comparable to those of control animals (Kinoshita et al., 1991). These findings suggest that formation of immunological memory and class switching are intact during vitamin A deficiency, despite an impaired IgM and IgG response to primary immunization. Human peripheral-blood lymphocytes from subjects previously immunized against tetanus toxoid were used to reconstitute control and vitamin A-deficient mice with severe combined immunodeficiency (SCID). After challenge with tetanus toxoid, vitamin A-deficient SCID mice had a 2.9-fold increase in human anti-tetanus toxoid antibody, compared with a 74-fold increase in control SCID mice (Molrine et al., 1995). In healthy children without vitamin A deficiency, vitamin A supplementation did not enhance antibody responses to tetanus toxoid (Kutukculer et al., 2000). These findings suggest that vitamin A supplementation is unlikely to enhance antibody responses in subjects who are not vitamin A-deficient.

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