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.
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.
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.
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.