Vitamin D deficiency and autoimmune diseases

Epidemiological evidence indicates a significant association between vitamin D deficiency and an increased incidence of autoimmune diseases. The presence of vitamin D receptors in the cells of the immune system and the fact that several of these cells produce the vitamin D hormone suggested that vitamin D could have immunoregulatory properties, and now potent immunomudulatory activities on dendritic cells, Th1 and Th17 cells, as well as B cells have been confirmed. Patients with undifferentiated connective tissue disease also show vitamin D deficiency and, interestingly, patients who progress into connective tissue diseases have lower vitamin D levels than those who remain in the undifferentiated connective tissue disease stage. Vitamin D deficiency and autoimmune diseases The recent study by Zold and colleagues [1] reports that a seasonal variance in levels of 25(OH)D3 was identified in patients with undifferentiated connective tissue disease (UCTD) and showed that these levels were, in any case, significantly lower than in controls during the corresponding seasons. The results showed also that more severe vitamin D deficiency in UCTD patients may play a role in the subsequent progress into well-defined connective tissue diseases (CTDs). Epidemiological evidence indicates a significant association between vitamin D deficiency and an increased incidence of autoimmune diseases [2]. Serum levels of vitamin D have been found to be significantly lower in patients with systemic lupus erythematosus (SLE) and type-1 diabetes mellitus than in the healthy population [3]. In addition, it was also found that lower levels of vitamin D were associated with higher disease activity in rheumatoid arthritis [4]. An inverse correlation has been described between the supplementation of vitamin D and the development of type-1 diabetes mellitus and multiple sclerosis [5]. Low serum levels of vitamin D3 might be partially related, among other factors, to prolonged daily darkness (reduced activation of pre-vitamin D by ultraviolet B sunlight), different genetic backgrounds (that is, vitamin D receptor polymorphism) and nutritional factors, and could explain the latitude-related prevalence of autoimmune diseases such as rheumatoid arthritis (RA) when considering the potential immunosuppressive roles of vitamin D [2]. Vitamin D or hormone D? The term vitamin D is, unfortunately, an imprecise term, referring to one or more members of a group of steroid molecules (seco-steroids). The A, B, C, and D ring structure is derived from the cyclopentanoperhydrophenanthrene ring structure of steroids. In particular, seco-steroids are those in which one of the rings has been broken [2]. Vitamin D, also known as cholecalciferol, is mainly generated in the skin of animals when one of the rings of the precursor molecule 7-dehydrocholesterol has been broken by ultraviolet B light (UV-B, sun light). Vitamin D (or hormone D) is thus not a true vitamin, because individuals with adequate exposure to sunlight do not require dietary supplementation. Although vitamin D is consumed in food, dietary intake alone is often insufficient, supplying only 20% of the body’s requirements [2]. Finally, the liver and kidney help convert vitamin D to its active hormone forms (vitamin D3 hormone). There is increasing evidence that steroid hormones (vitamins D2 and D3) derived from vitamin D act through classic nuclear receptors (nuclear vitamin D receptors (VDRs)), as well as specific binding sites on the plasma membrane of target cells that are coupled to signal transduction systems. Clarification of the physiological role of endogenous VDR Editorial Vitamin D or hormone D deficiency in autoimmune rheumatic diseases, including undifferentiated connective tissue disease