Impact of Vitamin A Supplementation on Immune System in Multiple Sclerosis Patients

• Serum levels of IL4, IL10, IFN γ, IL2, IL12 [ Time Frame: first day and after 6 month ] [ Designated as safety issue: No ]
  

• PBMC supernatant levels of IL4, IL10, IFN γ, IL2, IL12 [ Time Frame: first day and after 6 month ] [ Designated as safety issue: No ]
  
• RBP/ TTR ratio [ Time Frame: first day and after 6 month ] [ Designated as safety issue: No ]
  
• lymphocyte proliferation assay (BrdU colorimetric) [ Time Frame: first day and after 6 month ] [ Designated as safety issue: No ]
  

Multiple Sclerosis (MS) is a chronic inflammatory disease where Th1 like responses from myelin-specific CD4+ T cells, as secretion of pro-inflammatory IFN-g, are believed to play a major role in the pathogenesis. The myelin-specific T cells that mediate tissue destruction in MS are believed to become activated outside the central nervous system (CNS) in lymphoid tissue and when they cross the blood brain barrier they will re-encounter their antigen. Immune deviation is the redirection of the immune response from most often Th1 like responses to Th2 like responses, even though the opposite can also occur. Vitamin A (VA) or VA-like analogs known as retinoids, are potent hormonal modifiers of type 1 or type 2 responses but a definitive description of their mechanism(s) of action is lacking. High level dietary vitamin A enhances Th2 cytokine production and IgA responses, and is likely to decrease Th1 cytokine production. Retinoic acid inhibits IL 12 production in activated macrophages, and RA pretreatment of macrophages reduces IFNγ production and increases IL4 production in antigen primed CD4 T cells. Supplemental treatment with vitamin A or retinoic acid (RA) decreases IFNγ and increases IL5, IL10, and IL4 production. Thus, vitamin A deficiency biases the immune response in a Th1 direction, whereas high level dietary vitamin A may bias the response in a Th2 direction.