This review focuses its attention on the influence of the Vitamin D Receptor and hepcidin expressions that can suggest the protection or severity of leprosy.
Genetic factors, such as the vitamin D receptor, the major histocompatibility complex region, chromosome 20, human toll-like receptors, the natural resistance-associated macrophage protein 1, the nucleotide-binding oligomerization domain containing 2, phosphate-regulating gene with homologies to endopeptidase on the X chromosome and the tyrosine kinase growth factor receptor-ErbB-2, contribute to both vitamin D status and leprosy.
Although genetic variants in tumor necrosis factor (TNF), mannose binding lectin (MBL), and the vitamin D receptor (VDR) have been associated with leprosy clinical outcomes, these findings have not been extensively validated.
Among the immune response elements involved in the pathogenesis of leprosy are the Toll-like receptors (TLRs), vitamin D receptor (VDR), natural killer cells (NK), and T cells.
The risk of leprosy occurrence conditioned by VDR polymorphism was investigated by stratifying the population of a highly endemic Brazilian region into negative and positive Mitsuda responses.