1α,25-Dihydroxyvitamin D3 inhibits CD40L-induced pro-inflammatory and immunomodulatory activity in Human Monocytes

The role of vitamin D supplementation on erectile function

“…In an animal study on diabetic rats, it was demonstrated that treatment with VD for 12 weeks increased the serum level of T in treatment groups. [26] In a clini- Abnormalities in calcium and phosphorus homeostasis [10,15] Bronchial asthma [4,7] Coronary artery disease [14,16] Erectile dysfunction [9,17,18] Heart failure [10,16] Hypertension [9,14] Hypogonadism [19][20][21][22] Impaired vascular endothelial and smooth muscle function [9,16] Increased immune or inflammatory response [23,24] Infertility [25,26] Metabolic syndrome [10,14,27] Osteoporosis [19,28,29] Peripheral vascular disease [15,30] Respiratory diseases [3,4] Wearing sunscreen clothes cal randomized controlled trial, which is the first on this topic in literature, Pilz et al [39] investigated the effect of VD supplementation on androgens in men. The results were significant and the researchers observed that overweight men with VDD had a clinically meaningful increase in serum T levels after VD supplementation for 1 year.…”

“…In research, it was shown that VD inhibits the expression of inflammatory cytokines in monocytes, including IL-1, IL-6, TNF-α, IL-8, and IL-12. [23,24] VD may directly protect endothelial cells against oxidative stress; and VDD may contribute adversely to ED through inflammation.…”

维生素d 在免疫反应和自身免疫性疾病特别是多发性硬化中的作用

“…Vitamin D is also important for the interaction of monocytes with T cells, since 1,25(OH) 2 D 3 reduces the CD40L-related production of proinflammatory cytokines such as IL-1 and TNF-. Upon interaction between 1,25(OH) 2 D 3 and CD40L, monocytes can reduce T cell proliferation and IFN- production, and elevate IL-10 synthesis [41] . [43] .…”

Immunomodulatory Effect of Vitamin D in Children with Allergic Diseases

“…What is more, it inhibits monocyte production of inflammatory cytokines such as IL-1, IL-6, IL-8, IL-12, and TNF-α [23,26]. It additionally inhibits dendritic cell (DC) differentiation and maturation, directing to immature phenotype.…”

“…However, there are two pathophysiological mechanisms in the development of atopic dermatitis: first, immunological mechanisms that influence the Th1/Th2 adaptive immune responses; vitamin D receptor agonists have been shown to impact on Th1 and Th2 cell function, suppress allergen-specific IgE synthesis, inhibit dendritic cell maturation and induce tolerogenic dendritic cells, and finally to induce regulatory CD4+CD25+25Foxp3+T cells. Second, injury of the skin barrier function [26,29,31]. Several recent studies have shown that infants with high level of sensitization had a decreased concentration of 25(OH)D levels [27,29,37].…”