Abstract
Abstract Vitamins A and D are highly interactive in their binding of receptor complexes RAR-RXR and VDR-RXR, which regulate genes essential for normal immune function. To determine how vitamins impact the immune response toward respiratory viruses, we employed mice deficient in vitamin A (VAD), vitamin D (VDD), or both. Analysis of virus-specific antibody-forming cells (AFCs) in VAD mice following influenza virus infection revealed a reduction in IgA-producing AFCs in the respiratory tract mucosa, a first line of defense against respiratory viruses. The IgG/IgA ratio was increased in VAD, but not VDD mice. Interestingly, in double-deficient mice, inhibition was exacerbated to the extent that there were virtually no detectable virus-specific AFCs in the lower respiratory tract. To determine if vitamin deficiencies impact antibody isotypes in humans, we examined blood samples from residents of Memphis, TN. A substantial fraction of individuals exhibited low levels of vitamin A, D or both. As in mice, vitamin A and IgA levels were correlated. When vitamin A was low, antibody isotypes encoded by CH genes at the 3’ end of the heavy chain locus (IgA and IgG2) were poorly represented relative to those encoded at the 5’ end (IgM, IgG3 and IgG1), indicating abnormal CH switching or improper maturation or stability of switched AFCs. Results help explain how vitamin deficiencies render humans vulnerable to respiratory virus disease and encourage rapid implementation of corrective measures.
Published Version
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