Retinoids and Immunity

Hayes, Colleen E.; Nashold, Faye E.; Gómez, F. Enrique; Hoag, Kathleen A.

doi:10.1007/978-3-642-58483-1_21

Cited by 8 publications

(2 citation statements)

References 114 publications

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“…4. Various aspects of vitamin A deficiency that relate to the immune response are summarised in a review by Hayes et al (1999).…”

Section: Differentiating and Proliferating Effects Of Retinoids On Immentioning

confidence: 99%

Effects of dietary retinoids and carotenoids on immune development

Rühl

2007

Proc. Nutr. Soc.

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Carotenoids and retinoids are groups of nutritionally-relevant compounds present in many foods of plant origin (carotenoids) and animal origin (mainly retinoids). Their levels in human subjects vary depending on the diversity and amount of the individual's nutrient intake. Some carotenoids and retinoids have been investigated for their effects on the immune system bothin vitroandin vivo. It has been shown that retinoids have the potential to mediate or induce proliferative and differentiating effects on several immune-competent cells, and various carotenoids are known to be inducers of immune function. The immune-modulating effects of retinoids have been well documented, while the effects of carotenoids on the immune system have not been investigated as extensively, because little is known about their molecular mechanism of action. The present review will mainly focus on the molecular mechanism of action of retinoids and particularly carotenoids, their nutritional origin and intake, their transfer from the maternal diet to the child and their effects or potential effects on the developing immune system.

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“…4. Various aspects of vitamin A deficiency that relate to the immune response are summarised in a review by Hayes et al (1999).…”

Section: Differentiating and Proliferating Effects Of Retinoids On Immentioning

confidence: 99%

Effects of dietary retinoids and carotenoids on immune development

Rühl

2007

Proc. Nutr. Soc.

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“…The immune-regulatory actions of vitamin A are believed to be mediated by the retinoic acid (RA) isomers [26]. The two major natural RA isomers, all-trans-RA (ATRA) and 9-cis RA, bind to and thereby activate RA receptor/retinoid X-receptor heterodimers, which regulate the transcription of RA-responsive genes [27].…”

Section: Introductionmentioning

confidence: 99%

Retinoic acid regulates Fas-induced apoptosis in Jurkat T cells: reversal of mitogen-mediated repression of Fas DISC assembly

Engedal

Auberger

Blomhoff

2008

Journal of Leukocyte Biology

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The effect of the immune regulator vitamin A on T cell death has been poorly characterized. In the present study, we demonstrate that an active metabolite of vitamin A, retinoic acid (RA), promotes cell death in Jurkat leukemic T cells by counteracting mitogen-mediated repression of Fas-induced apoptosis. The effect of RA was dose-dependent, and at the optimal concentration of 1 muM, repression of Fas-induced cell death by the mitogens 12-O-tetradecanoylphorbol 13-acetate (TPA) or Con A was reversed by approximately 50% and 30%, respectively. RA promoted apoptosis rather than necrosis, as judged by analysis of cell morphology, mitochondrial membrane depolarization, and DNA fragmentation. TPA-mediated protection from Fas-induced apoptosis is dependent on ERK and NF-kappaB. However, analyses of ERK and NF-kappaB activities and expression of target genes indicated that RA-mediated counteraction of the protective effect of TPA did not involve negative crosstalk with ERK or NF-kappaB survival pathways. RA-induced cell death was accompanied by enhanced cleavage of procaspase-3, -6, and -8, as well as enhanced cleavage of DNA fragmentation factor 45. Interestingly, RA-mediated cleavage of procaspase-8 occurred very early and before any effect of RA could be detected on procaspase-3 cleavage, suggesting that RA might act at the level of the Fas death-inducing signaling complex (DISC). Indeed, DISC immunoprecipitation studies revealed that RA treatment reversed the inhibitory effect of TPA on CH11-induced recruitment and processing of procaspase-8 at the DISC. In conclusion, we have identified a role of RA in abrogating mitogen-mediated repression of Fas DISC assembly, thus enhancing Fas-induced apoptosis in leukemic T cells.

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Retinoid ameliorates experimental autoimmune myositis, with modulation of Th cell differentiation and antibody production in vivo

Ohyanagi¹,

Ishido²,

Suzuki³

et al. 2009

Arthritis & Rheumatism

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Objective. Polymyositis and dermatomyositis are chronic inflammatory muscle diseases. Retinoids are compounds that bind to the retinoic acid binding site of retinoic acid receptors and have biologic activities similar to those of vitamin A. Recent studies indicate that retinoids promote Th2 differentiation and suppress Th1 and Th17 differentiation in vitro. The present study was undertaken to examine the effects of a synthetic retinoid, Am80, on experimental autoimmune myositis as well as on Th phenotype development and antibody production.Methods. Experimental autoimmune myositis was induced in SJL/J mice by immunization with rabbit myosin. Am80 was administered orally once daily. Its effects were evaluated by measurement of the numbers of infiltrating inflammatory cells, production of inflammatory cytokines in muscle, production of Th-specific cytokines by myosin-stimulated splenic T cells, and production of antimyosin antibodies in serum.Results. In mice with experimental autoimmune myositis, orally administered Am80 significantly reduced the number of infiltrating inflammatory cells and the expression of tumor necrosis factor ␣ and interleukin-1␤ (IL-1␤) in muscle. Moreover, Am80 increased production of interferon-␥, IL-4, and IL-10, but not IL-17, by myosin-stimulated splenic T cells of mice with experimental autoimmune myositis, suggesting that it could enhance differentiation into Th1 and Th2, but not Th17, in vivo. Am80 also decreased serum levels of IgG2a and IgG2b antimyosin antibodies, but did not affect levels of IgG1 antimyosin antibodies. In addition, it suppressed chemokine expression and activator protein 1 activity in myoblasts in vitro. Conclusion. The synthetic retinoid Am80 has an inhibitory effect on experimental autoimmune myositis. It might regulate the development of Th phenotype and antibody production in vivo, in addition to its effects on cytokine and chemokine production.

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Retinoids and Immunity

Cited by 8 publications

References 114 publications

Effects of dietary retinoids and carotenoids on immune development

Effects of dietary retinoids and carotenoids on immune development

Retinoic acid regulates Fas-induced apoptosis in Jurkat T cells: reversal of mitogen-mediated repression of Fas DISC assembly

Retinoid ameliorates experimental autoimmune myositis, with modulation of Th cell differentiation and antibody production in vivo

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