Roles of Retinoic Acid in Induction of Immunity and Immune Tolerance

Kim, Chang H.

doi:10.2174/187153008786848312

Cited by 23 publications

(13 citation statements)

References 67 publications

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“…Decreased immunity to pathogens is associated with defective production of the mucosal antibody IgA and defective expression of gut-homing receptors by T and B cells (Iwata et al, 2004;Mora et al, 2006;Tokuyama, 1993, 1999). RA steers the differentiation of T and B cells in the direction to promote both immunity and immune tolerance (Kim, 2008). Induction of immune tolerance by RA is through several different mechanisms including induction of FoxP3 þ T cells (Benson et al, 2007;Coombes et al, 2007;Elias et al, 2008;Jaensson et al, 2008;Kang et al, 2007;Sun et al, 2007).…”

Section: Retinol Retinalmentioning

confidence: 99%

“…Induction of immune tolerance by RA is through several different mechanisms including induction of FoxP3 þ T cells (Benson et al, 2007;Coombes et al, 2007;Elias et al, 2008;Jaensson et al, 2008;Kang et al, 2007;Sun et al, 2007). Enhancement of immunity is mediated, in part, through its action on production of phagocytes and regulation of the effector lymphocyte trafficking (Kim, 2008;Mora and von Andrian, 2009;Ongsakul et al, 1985).…”

Section: Retinol Retinalmentioning

confidence: 99%

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Retinoic Acid, Immunity, and Inflammation

Kim

2011

Vitamins &Amp; Hormones

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Section: Retinol Retinalmentioning

confidence: 99%

Section: Retinol Retinalmentioning

confidence: 99%

Retinoic Acid, Immunity, and Inflammation

Kim

2011

Vitamins &Amp; Hormones

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“…Recently, there has been significant progress in elucidating the roles of RA in the regulation of immune cell activities [21–23, 45–48]. In the present study, we investigated the role of RA in the expression regulation of CD300B, a novel member of the leukocytes surface molecule family, and we also investigated the putative signaling pathways involved in the regulation of CD300B expression.…”

Section: Discussionmentioning

confidence: 99%

All-trans-retinoic acid and Erk1/2 signaling synergistically regulate the expression of CD300B in human monocytic cells

Chen

Pai

et al. 2011

Cellular Immunology

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The regulation of the cell-surface receptors that constitute the gene cluster, CD300, also known as the Myeloid Activating/Inhibitory Receptor (MAIR) family, is poorly understood. In the present study, we tested the hypothesis that all-trans-RA (RA), a bioactive form of vitamin A long recognized for its role in regulation of immune cell activities, may be a potent regulator of the expression of human CD300B. In monocytic THP-1 cells, RA (20 nM) alone significantly increased CD300B mRNA within 2 h and up to 20-fold after 24 h; however, CD300B protein determined by flow cytometry and confocal microscopy showed little change. A search for coactivating molecules revealed that phorbol myristyl acetate (PMA), a mimetic of diacylglycerol, alone increased CD300B mRNA by less than 5-fold; however, the combination of at-RA and PMA increased CD300B mRNA nearly 60-fold. Moreover, CD300B protein was increased. CD300B molecules were mainly located on the plasma membrane and in the endosomal compartment, sharing a distribution/recycling pattern similar to transferrin receptor CD71. The induction of CD300B mRNA by PMA required signaling through the MEK/ERK branch of the MAP kinase pathway, as PD98059, a MEK1/2 inhibitor, abrogated this response, while SB203580, an inhibitor of the p38 pathway, had no effect. Our data suggest a model in which RA alone induces a CD300B mRNA response in which transcripts accumulate but remain untranslated and therefore “sterile,” whereas RA combined with signals from the ERK1/2 pathway results in both increased CD300B transcription and protein expression on the cell surface and in endocytic vesicles.

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“…Additionally, RA appears to be required for the production of mature phagocytes in the bone marrow through its effects on MHC class II and co-stimulatory molecule expression [47]. Therapeutically, RA has long been used to treat myeloid leukemia given that it promotes myeloid cell differentiation and maturation [48,49].…”

Section: Introductionmentioning

confidence: 99%

Continuous retinoic acid induces the differentiation of mature regulatory monocytes but fails to induce regulatory dendritic cells

et al. 2014

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BackgroundMyeloid cells (MC) have potent immunoregulatory abilities that can be therapeutically useful to treat inflammatory disease. However, the factors which promote regulatory myeloid cell differentiation remain poorly understood. We have previously shown that estriol (E3) induces mature regulatory dendritic cells in vivo. To determine whether additional steroid hormones could induce mature regulatory myeloid cells, we investigated the effects of retinoic acid (RA) on MCs. Retinoic acid is a steroid hormone important in regulating mucosal immunity in the gut and promoting myeloid differentiation. We hypothesized that the presence of RA during differentiation would promote the formation of mature regulatory myeloid cells (MCregs).MethodsTo determine RA’s ability to induce regulatory myeloid cells, we differentiated bone marrow progenitor cells with granulocytic-macrophage colony-stimulating factor (GM-CSF) under the influence of RA. We found that day 7 MCs differentiated in the presence of RA had an increase in the percent positive and relative expression levels of both maturation (CD80, CD86, and MHCII) and inhibitory (PD-L1 and PD-L2) markers compared to control cells. Functionally, these day 7 RA MCs expressed increased intracellular IL-10, induced regulatory T cells in vitro compared to controls and suppressed the proliferation of responder immune cells even after inflammatory challenge with LPS.ConclusionRA induced mature regulatory myeloid cells that were suppressive and had a CD11b+ CD11c-Ly6C low/intermediate monocyte phenotype. Surprisingly, RA CD11c+ dendritic cells were not suppressive and could contribute to enhanced proliferation. These results suggest that continuous RA has unique effects on different myeloid populations during monopoeisis and dendropoiesis and promotes a population of regulatory monocytes.

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Roles of Retinoic Acid in Induction of Immunity and Immune Tolerance

Cited by 23 publications

References 67 publications

Retinoic Acid, Immunity, and Inflammation

Retinoic Acid, Immunity, and Inflammation

All-trans-retinoic acid and Erk1/2 signaling synergistically regulate the expression of CD300B in human monocytic cells

Continuous retinoic acid induces the differentiation of mature regulatory monocytes but fails to induce regulatory dendritic cells

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