IL-23 Receptor Expression on T Helper 17 Cells and its Implication in Multiple Sclerosis Relapse

Document Type : New and original researches in the field of Microbiology.

Authors

1 Medical Microbiology and Immunology, Faculty of Medicine, Ain Shams University

2 Medical Microbiology and Immunology department, Faculty of Medicine, Ain Shams University.

3 Neurology department, Faculty of Medicine, Ain Shams University.

4 Medical Microbiology and Immunology department, Faculty of Medicine Ain Shams university

Abstract

Background: Multiple Sclerosis (MS) is considered the prototype of neurodegenerative diseases affecting around 2 million people worldwide. MS was marked primarily as an IL-17-mediated autoimmune disease, the hallmark cytokine of T helper (Th) 17 cells. Th 17 cells are considered as one of MS key effectors through the IL-23/IL-17 axis. Objectives: To investigate IL-23 receptor expression on Th17 cells with assessment of serum IL-17 level and their implication in MS relapse. Methodology: Patients included 22 MS patients in remission, 22 MS patients in active relapse and 22 healthy controls. Clinical assessment of the expanded disability severity scale (EDSS) for included patients. All groups were subjected to flow-cytometric analysis to assess expression of IL-23 receptor (IL-23R) on CD4+ T cells and measurement of serum IL-17A level by using ELISA. Results: MS patients during active relapse had a higher IL-17A serum level, and a higher percentage of IL-23R+ CD4+ T cells with increased IL-23R expression density on CD4+ T cells compared to patients in remission and controls. Conclusion:  The results reflected Th 17 key role in MS immune pathogenesis. Thus, the IL-23/IL-17 axis can be a potential target for immunomodulatory therapies ameliorating the Th17 mediated autoimmunity through novel treatments for those patients.

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