Rheumatoid arthritis (RA) is a systemic multifactorial autoimmune disorder. The interactions between diverse environmental and genetic factors lead to the onset of this complex autoimmune disorder. Serum levels of vitamin D (VD) are involved in the regulation of various immune responses. Vitamin D is a key signaling molecule in the human body that maintains calcium as well as phosphate homeostasis. It also regulates the functions of the immune system and, thus, can play a substantial role in the etiology of various autoimmune disorders, including RA. Low serum VD levels have been found to be associated with a higher risk of RA, although this finding has not been replicated consistently. The molecular mechanisms by which VD influences autoimmunity need to be further explored to understand how variation in plasma VD levels could affect the pathogenesis of RA. This mini-review focuses on the influence of VD and its serum levels on RA susceptibility, RA-associated complexities, treatment, and transcriptome products of key proinflammatory cytokines, along with other cytokines that are key regulators of inflammation in rheumatoid joints.

Rheumatoid arthritis is categorized as a systematic autoimmune disease which causes chronic disabilities exclusively in bones that are aligned with synovium. RA aetiology is still unknown but previous studies have coined that several number of factors play a significant role e.g. environmental and genetic factors. Cellular signalling pathways orchestrate the inflammatory response that regulates various cellular functions like cellular progression, proliferation, death and secretion of signalling molecules (pro and anti-inflammatory cytokines) in response to genetic and environmental stimuli. These regulatory pathways are tightly controlled Rheumatoid arthritis is categorized as a systematic autoimmune disease which causes chronic disabilities exclusively in bones that are aligned with synovium. RA aetiology is still unknown but previous studies have coined that several number of factors play a significant role e.g. environmental and genetic factors. Cellular signalling pathways orchestrate the inflammatory response that regulates various cellular functions like cellular progression, proliferation, death and secretion of signalling molecules (pro and anti-inflammatory cytokines) in response to genetic and environmental stimuli. These regulatory pathways are tightly controlled and naturally activated by ligands that attach to their respective receptors on the cell surface. In diseased state, these signalling pathways escape the normal control mechanisms, resulting in intensification of cytokines and chemokines, transcription factors and mediatory proteins that disrupt normal cell processes and might bring about auto-destructive consequences such as in the case of rheumatoid arthritis. The review highlights multiple levels of targeting molecules in signalling pathways that may be potential diagnostic markers and also attempts to underline potential therapeutic targets.and naturally activated by ligands that attach to their respective receptors on the cell surface. In diseased state, these signalling pathways escape the normal control mechanisms, resulting in intensification of cytokines and chemokines, transcription factors and mediatory proteins that disrupt normal cell processes and might bring about auto-destructive consequences such as in the case of rheumatoid arthritis. The review highlights multiple levels of targeting molecules in signalling pathways that may be potential diagnostic markers and also attempts to underline potential therapeutic targets.

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The spectrum of rheumatic disease is wide and includes conditions with diverse pathology, although most have in common a heritable risk with a complex genetic basis. Over the past decade intense efforts have been done to understand the contribution of genotype to the expression of disease in terms of both basic pathogenesis and clinical characteristics. The dramatic improvement in technology and methodology has accelerated the pace of gene discovery in complex disorders in an exponential fashion. This review focuses on rheumatoid arthritis and describes some of the recently described genes that underlie this condition and the extent to which they overlap.