Thus, it appears that 1,25(OH) 2D 3 upregulates antimicrobial peptide production, primarily cathelicidin, on a variety of different cells. Treatment with 1,25(OH) 2D 3 upregulates cathelicidin mRNA in several cell lines. The killing mechanism of cathelicidin involves bacterial lysis by destabilizing cell membrane. Cathelicidin has broad antimicrobial activity against Gram-positive and Gram-negative bacteria, as well as certain viruses and fungi. Cells of the immune system including neutrophils and macrophages and cells lining epithelial surfaces that are constantly exposed to potential pathogens such as the skin, the respiratory, and the gastrointestinal tract produce cathelicidin. Humans have only one cathelicidin, which is cleaved to form LL-37. Vitamin D enhances the production of defensin ОІ2 and cathelicidin in response to infection by macrophages, monocytes, and keratinocytes. demonstrated in the 1980s that 1,25(OH) 2D 3 inhibited the proliferation of Mycobacterium tuberculosisin culture. Thereafter, several groups used vitamin D 2 and D 3 as a treatment for tuberculosis. Alfred Windaus contributed to the discovery of the chemical structure of vitamin D 2 and vitamin D 3 found in cod-liver-oil and received the Nobel prize. Fifty years later, Niels Finsen received the third Nobel Prize in Medicine for his description of using UV light, an effective method to increase vitamin D status, to treat lupus vulgaris, a cutaneous form of tuberculosis. In 1849, Williams reported favorable results with the use of cod-liver-oil, an excellent source of vitamin D, in the treatment of patients with tuberculosis. Vitamin D has been used as a treatment of infections for more than 150В years. The first data on the effect of vitamin D on the innate immune system have been generated on the treatment of diseases caused by mycobacteria, such as tuberculosis and leprosy. Vitamin D is a regulator of the innate immune system. The innate immune system is a first line of defense against infection. Vitamin D is involved in the regulation of the innate immunity as it enhances the defense system of the organism against microbes and other pathogenic organisms, and it modulates the adaptive immune system through direct effects on T-cell activation and on the phenotype and function of antigen-presenting cells, particularly dendritic cells.Дў.1 Vitamin D and the innate immune system Cells of the immune system, which express the VDR and harbor 1-О±-hydroxylase, are macrophages, T cells, dendritic cells, monocytes, and B cells ( Figure 1). The extra-renal 1-О±-hydroxylase is not upregulated by PTH, and thus, production of 1,25(OH) 2D 3 is dependent on concentrations of the substrate 25(OH)D 3, and it may be regulated by inflammatory signals, such as lipopolysaccharide and cytokines. Thus, cells of the immune system respond to vitamin D and also activate vitamin D in a paracrine or autocrine fashion. Various cells of the immune system also express the VDR and harbor 1-О±-hydroxylase. However, various cells express the vitamin D receptor (VDR) and the vitamin D activating enzyme 1-О±-hydroxylase. The classic function of vitamin D is to enhance intestinal absorption of calcium by regulating several calcium transport proteins in the small intestine. Optimal vitamin D levels appear to be required for normal immune function and for the prevention and treatment of autoimmune diseases. Low vitamin D levels have been observed in patients with systemic sclerosis, especially in the diffuse form of the disease. Low vitamin D levels have also been observed in patients with autoimmune HashimotoвЂ™s thyroiditis. Vitamin D deficiency is also observed in patients with inflammatory bowel disease and may be related to disease severity. Vitamin D should be administered to patients with multiple sclerosis, and this seems to mitigate the symptoms of the disease and to prevent disease progression. Vitamin D deficiency is also related to the development and the severity of multiple sclerosis. SLE develops in patients with vitamin D deficiency, and the activity of the disease is also greater in patients with vitamin D deficiency. Vitamin D deficiency is also related to the development of systemic lupus erythematosus (SLE). RA develops in patients with vitamin D deficiency, and the activity of the disease is related to vitamin D deficiency. In particular, vitamin D deficiency is related to the development and the severity of rheumatoid arthritis (RA). Vitamin D deficiency is known to be related to the development of autoimmune diseases. Vitamin D has many and profound effects on the immune system.

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