PMC:7647877 / 34625-36563 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7647877","sourcedb":"PMC","sourceid":"7647877","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7647877","text":"Vitamin A deficiency impairs barrier function, impairs immune responses and increases susceptibility to a variety of infections. Furthermore, many aspects of innate immunity, in addition to barrier function, are affected by vitamin A. For example, vitamin A regulates the number and function of NK cells [82], contributes to the phagocytic and oxidative activity of the macrophage burst [79] and controls the maturation of neutrophils and its deficiency [83]. The activity of natural killer cells is therefore reduced by vitamin A deficiency. The impact of vitamin A on acquired immunity is however clear since it is involved in the development and differentiation of Th1 and Th2 cells [62, 79]. Moreover there is evidence that vitamin A deficiency alters the balance of Th1 and Th2 cells, decreasing the Th2 response, without affecting or, in some cases, enhancing the Th1 response. This suggests that vitamin A increases the Th1 cell average in immunity [84]. However, studies in several experimental models have shown how the retinoic acid metabolite of vitamin A reduces the responses of Th1-type cells (cytokines, cytokine receptors and the transcription factor T-bet, which promotes Th1), improving responses to Th2-type cells (cytokines and Th2-favoring transcription factor GATA-3) [62]. Indeed, it maintains the normal Th2 response mediated by antibodies by suppressing the production of IL-12, TNF-α and IFN-γ by Th1 cells [85]. Vitamin A appears to be important in the differentiation of regulatory T lymphocytes by suppressing Th17 differentiation, which have implications for the control of adverse immune reactions [86]. It helps regulate the production of IL-2 and the pro-inflammatory TNF-γ, which activates the phagocytic and oxidative action of the macrophages activated during inflammation [79]. It ensures the normal functioning of B lymphocytes, necessary for the generation of antibody responses to the antigen 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