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Although Vitamin D is believed to be involved in a large number of immuneresponses our understanding of these processes at cellular level remained atinfancy. We develop and solve a coarse grained kinetic network model toquantify the effects of variation of vitamin D on human immunity. The system ofequations accounts for known inter-relation between active and inactive vitaminD, antigen presenting cells, effector T cells, regulatory T cells and pathogen.Both time dependent and steady state solutions are obtained. The time dependentsolution of the system of equations reveals that the immune response is ratherstrongly regulated in presence of vitamin D. We found quantitatively that lowerthan optimum levels of concentration of active vitamin D correspond to weakregulation where, once a pathogen/antigen enters the body, the nature of theimmune response would be less regulatory and hence more aggressive, orinflammatory. The steady state solution of our model shows that vitamin Denhances the tolerance level of immune system, thereby increasing resistance toautoimmune diseases. Our model and accompanied numerical analyses revealanother important aspect of immunity: While extremely low levels of vitamin Dcould lead to increased risk of autoimmune responses, an overdose (toxic) levelwould give rise to too large a tolerant response, leading to the increased riskof tumors and cancerous cell growth.

Vitamin D sensitivity to the immune responses and autoimmunity: A chemical network model study