Antibody production in vitamin A‐depleted rats is impaired after immunization with bacterial polysaccharide or protein antigens

Pasatiempo, A. M. G.; Kinoshita, M; Taylor, Christopher E.; Ross, A. Catharine

doi:10.1096/fasebj.4.8.2110538

Cited by 91 publications

(48 citation statements)

References 40 publications

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“…The synthesis of antibodies to T-cell-dependent antigens is typically depressed during vitamin A deficiency, as shown in several animal models (58,100,140,158). The evidence for an association between vitamin A status and T-cell-dependent antibody response is reviewed below.…”

Section: T-cell-dependent Humoral Responsesmentioning

confidence: 99%

Effects of Vitamin A Supplementation on Immune Responses and Correlation with Clinical Outcomes

2005

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Vitamin A supplementation to preschool children is known to decrease the risks of mortality and morbidity from some forms of diarrhea, measles, human immunodeficiency virus (HIV) infection, and malaria. These effects are likely to be the result of the actions of vitamin A on immunity. Some of the immunomodulatory mechanisms of vitamin A have been described in clinical trials and can be correlated with clinical outcomes of supplementation. The effects on morbidity from measles are related to enhanced antibody production and lymphocyte proliferation. Benefits for severe diarrhea could be attributable to the functions of vitamin A in sustaining the integrity of mucosal epithelia in the gut, whereas positive effects among HIV-infected children could also be related to increased T-cell lymphopoiesis. There is no conclusive evidence for a direct effect of vitamin A supplementation on cytokine production or lymphocyte activation. Under certain circumstances, vitamin A supplementation to infants has the potential to improve the antibody response to some vaccines, including tetanus and diphtheria toxoids and measles. There is limited research on the effects of vitamin A supplementation to adults and the elderly on their immune function; currently available data provide no consistent evidence for beneficial effects. Additional studies with these age groups are needed

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Section: T-cell-dependent Humoral Responsesmentioning

confidence: 99%

Effects of Vitamin A Supplementation on Immune Responses and Correlation with Clinical Outcomes

2005

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“…ATRA is required for optimal production of neutrophils, NK (natural killer) cells and B-cells [28], and it can promote humoral immune responses to pathogens [29,30].…”

Section: Introductionmentioning

confidence: 99%

all-trans-Retinoic acid improves immunocompetence in a murine model of lipopolysaccharide-induced immunosuppression

et al. 2013

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Secondary infections due to post-sepsis immunosuppression are a major cause of death in patients with sepsis. Strategies aimed at restoring immune functions offer a new perspective in the treatment of sepsis. In the present study, we used LPS (lipopolysaccharide)-immunosuppressed mice to analyse the effects of ATRA (all-trans retinoic acid) on different immune parameters. The IS (immunocompromised) group had decreased lymphocyte and increased MDSC (myeloid-derived suppressor cell) counts in lymph nodes. They also had an impaired in vitro T-cell proliferation, mediated by MDSCs. ATRA administration restored T-cell proliferation, which was associated with a decreased number of live MDSCs. The IS group treated with ATRA had an increased number of CD4+ and CD8+ T-cells. ATRA partially improved the primary humoral immune response, even when immunosuppression was established first and ATRA was administered subsequently. Our results demonstrate that ATRA restores immunocompetence by modulating the number of leucocytes and the survival of MDSCs, and thus represents an additional potential strategy in the treatment of the immunosuppressive state of sepsis.

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“…and type 2 (polysaccharide) antigens [5]. The secondary response to tetanus toxoid also was very low in VA-deficient rats [6,7].…”

mentioning

confidence: 95%

Retinoic Acid and Polyriboinosinic Acid Act Synergistically to Enhance the Antibody Response to Tetanus Toxoid during Vitamin A Deficiency: Possible Involvement of Interleukin‐2 Receptor‐β, Signal Transducer and Activator of Transcription‐1, and Interferon Regulatory Factor‐1

DeCicco

Zolfaghari

et al. 2000

J INFECT DIS

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Antibody responses to T cell-dependent antigens are reduced during vitamin A (VA) deficiency and restored by retinoids. To test whether retinoic acid (RA) and polyinosinic:polycytidylic acid (PIC), an inducer of interferons, can increase specific antibody production, VA-deficient rats were treated with all-trans-RA, PIC, or both at the time of primary immunization with tetanus toxoid. VA-deficient rats produced low primary and secondary anti-tetanus IgG responses (P<.001 vs. VA-sufficient controls). Both responses were increased synergistically by RA plus PIC (P<.0001). In VA-deficient spleens, mRNAs were low for interleukin (IL)-2 receptor-beta, interferon regulatory factor-1, and signal transducer and activator of transcription 1. Each, however, was induced by RA plus PIC (P<.0001 vs. controls). Conversely, IL-12 and IL-10 mRNAs were elevated in VA deficiency and were induced by PIC and suppressed by RA. Thus, RA plus PIC appears to be a promising combination for stimulating antigen-specific immunity. Several molecular factors identified here may partially account for the observed enhancement.

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Antibody production in vitamin A‐depleted rats is impaired after immunization with bacterial polysaccharide or protein antigens

Cited by 91 publications

References 40 publications

Effects of Vitamin A Supplementation on Immune Responses and Correlation with Clinical Outcomes

Effects of Vitamin A Supplementation on Immune Responses and Correlation with Clinical Outcomes

all-trans-Retinoic acid improves immunocompetence in a murine model of lipopolysaccharide-induced immunosuppression

Retinoic Acid and Polyriboinosinic Acid Act Synergistically to Enhance the Antibody Response to Tetanus Toxoid during Vitamin A Deficiency: Possible Involvement of Interleukin‐2 Receptor‐β, Signal Transducer and Activator of Transcription‐1, and Interferon Regulatory Factor‐1

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