T lymphocytes

Vitamin A appears to modulate the balance between T-helper type 1- and T-helper type 2-like responses. Trichinella spiralis infection in mice usually stimulates strong T-helper type 2-like responses, characterized by parasite-specific IgG responses and a cytokine profile dominated by interleukin (IL)-4, IL-5 and IL-10 production. However, in vitamin A-deficient mice, infection by T. spiralis results in low production of parasite-specific IgG and a cytokine profile dominated by interferon (IFN)-7 and IL-12 production, more characteristic of a T-helper-1 profile (Carman et al., 1992; Cantorna et al., 1994, 1996). Lymphocyte responsiveness to stimulation by concanavalin A or p-lactoglobulin was higher and production of IL-2 and IFN-7 was higher in lymphocyte supernatants from vitamin A-deficient rats, compared with control rats, further supporting the idea that vitamin A deficiency modulates a shift towards T-helper type 1-like responses (Wiedermann et al., 1993b). Vitamin A appears to inhibit production of IFN-7, IL-2 and granulocyte-macrophage colony-stimulating factor (GM-CSF) by type 1 lymphocytes in vitro (Frankenburg et al., 1998). The effect of high-level dietary vitamin A on the shift to T-helper type 2-like responses in BALB/c mice has been used to explain the apparent lack of benefit of vitamin A supplementation for acute lower respiratory infections in humans (Cui et al., 2000).

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