Vitamin D, a fat-soluble vitamin, needed for calcium absorption and well known for its role in maintaining bone health, has garnered substantial interest in recent times for its conjectural role in the pathogenesis and immunomodulation in autoimmune rheumatic diseases (AIRDs). The fact that vitamin D receptors are present on a vast multitude of cells including macrophages, dendritic cells, B cells and T cells in the body is in itself indicative of its multifarious role in immune regulation. There have been studies that clearly suggest vitamin D curtails antigen-presenting cells (APC) maturation, augments regulatory T cells and decreases pro-inflammatory cytokines, thereby establishing immune tolerance. This immunomodulatory function of vitamin D has been implicated in multiple AIRDs like rheumatoid arthritis (RA), systemic lupus erythematous (SLE), Sjogren’s syndrome, spondyloarthropathies, vasculitis and others, and its deficiency has been shown to be positively linked to both occurrence and severity of AIRDs. In addition to influencing adaptive immunity by inhibiting Th1 mediated cytokine storm, shifting response from Th1 to Th2, vitamin D also plays a role in altering the innate immune response by increasing production of antimicrobial peptides, promoting phagocytosis and regulating the Toll-like receptors (TLRs). The current treatment guidelines regarding management of vitamin D deficiency in adults involve achieving serum 25(OH)D levels of at least 30 ng/mL through supplementation, with higher doses recommended for individuals in high-latitude regions or with hyper-pigmented skin. Vitamin D has shown promise in helping mitigate the burden of AIRDs in both occurrence and severity aspect. However, further clinical and randomised control trials are needed to lay down a uniform and definite evidence in treatment protocol.