Immunopathology of multiple sclerosis

  Multiple sclerosis (MS), an inflammatory disorder of central nervous system (CNS), is the most common cause of neurological disability especially in young adults. The disorder results from interplay between unidentified genetic and environmental factors. In MS, cells of immune system attack myelin, progressive loss of certain body function and physical ability occur. In severe cases, the progression of disease leads to permanent damage. The auto-reactive peripheral CD4+ T cells recognize auto-antigen within CNS parenchyma and polarize toward Th1 phenotype. Activated Th1 cells cause myelin disruption and release of new potential CNS auto- antigen. Pro-inflammatory cytokines such as interferon- g , TNF- a and chemokines which is secreted by Th1 cells induce additional unspecific inflammatory cells and specific anti myelin antibody-forming B cells that amplify tissue injury. Finally, the apoptotic death of the T cells or conversion of the T cells toward Th2 phenotype positively modulates the outcome of the lesions in CNS .   Clinical manifestation of the disease is classified in three types, primary: direct damage (weakness, tremors, tingling,etc) secondary: result of primary (paralysis lead to bedsores and bladder/urinary incontinence problems) tertiary: social, psychological and vocational complication (depression is very common).   The aims of treatment are: reduction of sickness attack (by corticosteroid, interferon beta 1b and 1a, glatriamer acetate, natalizumab, etc) and reduction of the disorder. The prospect of the potential tools to prevent MS is tempting, yet challenging to investigate studies about roll of vitamin D in reduction of development of disease. Intensive research on MS provides a promising prospective of the disease management in the future.