The Role of Vitamin D Receptor in Innate and Adaptive Immunity: A Study in Hereditary Vitamin D–Resistant Rickets Patients

Abstract

Our results demonstrate impairments in various components of innate immunity in HVDTRR patients' monocytes and a proinflammatory cytokine profile in their lymphocytes. The underlying VDR-independent compensatory mechanisms that protect HVDRR patients from infections and autoimmune diseases remain undetermined.

A human vitamin D receptor mutation causes rickets and impaired Th1/Th17 responses

“…Our patient with HVDRR did not respond to vitamin D stimulation in terms of pro-inflammatory (Th1 and Th17) and anti-inflammatory (Th2) cell markers, whereas his parents demonstrate a 1,25-(OH) 2 D 3 -initiated reduction of Th1 and Th17 cell markers and induction of Th2/Treg markers. In concordance with our data, impairments in a proinflammatory cytokine profile in lymphocytes of HVDRR patients were recently reported by Tiosano and colleagues [22]. These findings indicate that the patient may be prone to immunogenic challenges.…”

Cardiometabolic Risks in Polycystic Ovary Syndrome: Non-Traditional Risk Factors and the Impact of Obesity

“…The findings are however inconsistent. Vitamin D also plays a crucial role in the modulation of innate and adaptive immune response in various inflammatory and autoimmune diseases [126,127] . It is now recognised that active metabolite vitamin D receptors are expressed in cells of the immune system [128] .…”

Vitamin D Nuclear Receptor and Periodontal Disease: A Review

“…At the same time, VDR suppresses interleukin (IL)-12 production and enhances IL-10 production in dendritic cells [17]. VDR regulates the production of T-cell helper 1 and 2 cytokines and IL-17, by which it influences adaptive immunity and inflammation [18]. Furthermore specific T-cell cytokines are able to influence the TLR-induced VDRdependent antimicrobial pathway in human monocytes.…”

“…Furthermore specific T-cell cytokines are able to influence the TLR-induced VDRdependent antimicrobial pathway in human monocytes. The TH1 cytokine interferon γ enhances the TLR2/1 induction of CYP27B1, cathelicidin [18]. Cathelicidins have significant broad antimicrobial activity against both gram-positive and gram-negative bacteria [17].…”