Control of Circulating IgE by the Vitamin D Receptor In Vivo Involves B Cell Intrinsic and Extrinsic Mechanisms

James, Jamaal L.; Weaver, Veronika; Cantorna, Margherita T.

doi:10.4049/jimmunol.1601213

Cited by 44 publications

(31 citation statements)

References 44 publications

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“…Thus, endogenous calcitriol from activated immune cells in lymphoid tissues is important in a paracrine and/or autocrine fashion for the immune functions of calcitriol, as discussed previously (1,31,32) and extending the knowledge to IgE regulation by genetic evidence. Moreover, VDR function in murine B lymphocytes, but not T lymphocytes, contributes to the control of sensitization-induced specific IgE, as shown recently in lymphocyte-specific KO mice (33). Thus, our data suggest that endogenous calcitriol from T cells acts on the VDR in B cells to reduce IgE in vivo.…”

Section: Discussionsupporting

confidence: 85%

Endogenous Calcitriol Synthesis Controls the Humoral IgE Response in Mice

Lindner

Treptow

Geldmeyer-Hilt

et al. 2017

The Journal of Immunology

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The vitamin D receptor participates in the control of IgE class-switch recombination in B cells. The physiologic vitamin D receptor agonist, 1,25(OH)D (calcitriol), is synthesized by the essential enzyme 25-hydroxyvitamin D-1α-hydroxylase (CYP27B1), which can be expressed by activated immune cells. The role of endogenous calcitriol synthesis for the regulation of IgE has not been proven. In this study, we investigated IgE-responses in -knockout (KO) mice following sensitization to OVA or intestinal infection with Specific Igs and plasmablasts were determined by ELISA and ELISpot, expression was measured by quantitative PCR. The data show elevated specific IgE and IgG1 concentrations in the blood of OVA-sensitizedKO mice compared with wild-type littermates (+898 and +219%). Accordingly, more OVA-specific IgG1-secreting cells are present in spleen and fewer in the bone marrow of -KO mice. Ag-specific mechanisms are suggested as the leucopoiesis is in general unchanged and activated murine B and T lymphocytes express Accordingly, elevated specific IgE concentrations in the blood of sensitized T cell-specific -KO mice support a lymphocyte-driven mechanism. In an independent IgE-inducing model, i.e., intestinal infection with, we validated the increase of total and specific IgE concentrations of -KO compared with wild-type mice, but not those of IgG1 or IgA. We conclude that endogenous calcitriol has an impact on the regulation of IgE in vivo. Our data provide genetic evidence supporting previous preclinical and clinical findings and suggest that vitamin D deficiency not only promotes bone diseases but also type I sensitization.

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Section: Discussionsupporting

confidence: 85%

Endogenous Calcitriol Synthesis Controls the Humoral IgE Response in Mice

Lindner

Treptow

Geldmeyer-Hilt

et al. 2017

The Journal of Immunology

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“…VD can maintain intestinal epithelial proliferation and turnover, inhibit intestinal epithelial apoptosis, alleviate structural damage, preserve intestinal barrier integrity and prevent intestinal barrier dysfunction. 40,41 Taking into consideration the association of VD deficiency/insufficiency with the development of allergy through the direct and indirect regulation of IgE production in B cells by VD receptors, 42 our data on the high The number of PA patients (n = 108) with…”

Section: Discussionmentioning

confidence: 99%

Pityriasis alba: Possible associations with intestinal helminths and pathogenic protozoa

Toychiev¹,

Mirzoeva

Davis³

et al. 2019

Int J Clin Pract

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Summary Background The aetiology of pityriasis alba (PA) remains uncertain, and children are at risk for PA and intestinal parasites. Aim To determine the prevalence of intestinal parasites in PA patients and to evaluate their possible role in PA pathogenesis. Methods Overall, 180 PA patients and 100 healthy individuals were enrolled. Intestinal parasites were diagnosed by triple coproscopy, and the total serum Immunoglobulin E (IgE) levels were determined by ELISA. PA patients with intestinal parasites were treated with conventional antiparasitic drugs. Patient response to antiparasitic therapy was evaluated after 6 weeks. Results The prevalence of intestinal parasites in PA patients and controls was 60 ± 3.6% and 32 ± 4.6%, respectively (P < .0001). Regardless of the parasite species among the PA patients and control individuals, the total IgE levels were significantly higher in PA patients (P ≤ .05). The highest values of IgE were found in PA patients with Hymenolepis nana (641.7 ± 46.3 IU/mL). The total IgE level in PA patients with parasites decreased after antiparasitic therapy, but the reduction was only significant in patients with H. nana (P < .05). Complete disappearance of hypopigmented patches was observed after the elimination of H. nana, Giardia lamblia and Enterobius vermicularis in 65 ± 10.6%, 48.7 ± 8.0% and 33.3 ± 8.2% of cases, respectively. In total, a positive clinical response to antiparasitic therapy was achieved in 60 ± 4.7% of infected PA patients. Conclusion A positive clinical response to antiparasitic therapy indicates the role of intestinal parasites in PA pathogenesis. Parasitological examination is justified by the recovery of 60 ± 4.7% of infected PA patients after the elimination of intestinal parasites.

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“…Similarly, murine models have shown that vitamin D deficiency exacerbates allergic reactions mediated by increased levels of specific-IgE and reduced percentages of Foxp3 + Tregs, as well as an altered intestinal epithelial barrier [129,130]. Vitamin D can directly control IgE production by a mechanism dependent on B cell-derived IL-10, although the effect of vitamin D on other cell types is also implicated in the regulation of IgE levels [131]. Deficiency of dietary vitamin A has also been associated with breaking of oral tolerance through decreased expression of RALDH in CD103 + DCs [132].…”

Section: Other Dietary Factorsmentioning

confidence: 99%

Immune Basis of Allergic Reactions to Food

Lozano‐Ojalvo

Berin

Tordesillas

2019

J Investig Allergol Clin Immunol

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Food allergies are diseases where the normal tolerance response to oral antigens is altered. Recent advances have begun to uncover mechanisms that mediate sensitization to food allergens and maintenance of the disease. Production of alarmins by epithelial cells triggers a cascade that leads to allergen-specific IgE synthesis. IL-9 has also been shown to play a role in mast cell recruitment and amplification of the allergic response. In recent years, increasing evidence suggests that sensitization to food allergens can be developed via nonoral routes, in particular the skin, thus leading to the "dual exposure hypothesis". Environmental factors such as diet or microbiota can shape the immune system to promote tolerance or sensitization to food antigens. While the mechanism of primary tolerance to food antigens is quite clear, that leading to permanent tolerance in food-allergic individuals through immunotherapy is still under study. Understanding the mechanisms by which oral tolerance is suppressed and sensitization develops will help to identify new targets to develop combined therapies for the treatment of food allergies.

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Control of Circulating IgE by the Vitamin D Receptor In Vivo Involves B Cell Intrinsic and Extrinsic Mechanisms

Cited by 44 publications

References 44 publications

Endogenous Calcitriol Synthesis Controls the Humoral IgE Response in Mice

Endogenous Calcitriol Synthesis Controls the Humoral IgE Response in Mice

Pityriasis alba: Possible associations with intestinal helminths and pathogenic protozoa

Immune Basis of Allergic Reactions to Food

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