Immunological mechanisms of multiple sclerosis and responses to therapy
Keywords:
immunomodulatory therapy, IL-17, multiple sclerosis, Th17 lymphocytesAbstract
Multiple sclerosis (MS) is a chronic autoimmune inflammatory neurodegenerative disease of the central nervous system (CNS) with an uncertain etiology. The prevalence of MS in Bulgaria is estimated at 44.5 per 100,000 people, which currently accounts for more than 3,600 patients in our country.
The role of Th17 cells is known for a large number of autoimmune diseases, including MS. The autoimmune nature of MS is confirmed by an experimental model of autoimmune encephalomyelitis, where Th17 lymphocytes play a key role. Th17 cells can be detected both in the CNS due to pathogenic processes locally and in peripheral blood in the presence of a disturbed blood-brain barrier. The IL-17 secreted by Th17 cells together with other cytokines such as IL-6, TNFα, IL-22 contribute to the maintenance of the inflammatory process and the demyelination of the neurons.
The world scientific community and the pharmaceutical industry are making long-term attempts to detect the causes of resistance of some patients to immunomodulatory treatment in MS. The question is also asked why, after a certain period of treatment, the therapy stops being effective and the disease progresses.
Considerable attention is paid to immunological markers, especially considering the autoimmune disease genesis. Increasingly popular is the measurement of expression of genes and levels of T-cells and cytokines. It is promising to monitor Th17 and Th22 cell counts as well as IL-6, IL-17A in treatment with beta interferons and fingolimod.
Studies in the field could supplement the data on the role of Th17 cells and their respective cytokines in predicting the risk of attacks or worsening of disease symptoms as well as to monitor the effect of immunomodulatory therapy in MS patients. This could inevitably improve the quality of life of the patients through reliable symptom and therapy control.
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Copyright (c) 2018 Marina Ivanova, E. Krasimirova, Ts. Velikova, I. Milanov, D. Kyurkchiev
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