Evaluation of Tumor Necrosis Factor Related Apoptosis Inducing Ligand (TRAIL) as a Response Marker for Interferon beta in Multiple Sclerosis

Nada, Maha ; Khaleel, Salma H ; Bayoumy, Iman M ; Ahmed, Rania 


Abstract


Background: Multiple sclerosis is the most common disease of the CNS that causes long and severe disability in young adults. Some patients with relapsing-remitting MS (RRMS) are unresponsive to IFN-β therapy. The Tumor necrosis factor Related Apoptosis Inducing Ligand (TRAIL) level was proposed as a response marker for IFN beta treatment. Objective: To recognize patients who will benefit most from treatment by assessing the functional relevance of TRAIL, to the clinical treatment response. Methods: This study was done on 24 patients from the Neurology department, Ain Shams University Hospitals. Patients had relapsing-remitting multiple sclerosis, for longer than 1 year. Patients were selected with no immunomodulatory treatment, and no exacerbations 4 weeks before start of study. Patients were examined clinically. MRI examinations were done before, 6 months and at the end of treatment. Estimation of TRAIL levels on monocytes and lymphocytes surfaces was done before treatment. Patients were given 44μg interferon beta 1a by subcutaneous injection three times per week for 1 year. Responders were defined as patients with no relapses and non-responders with one or more relapses during treatment (one year). Results: Responders showed higher values in the number of lymphocytes and monocytes having TRAIL and in the amount of TRAIL on them. Clinically worse patients showed higher number of monocytes having TRAIL. Conclusion: All the markers of TRAIL were increased in the responder group .The monocyte level was increased in clinically worse patients, which suggests that monocytes can be a better marker than lymphocytes


Other data

Keywords TRAIL;Multiple Sclerosis;Interferon beta
Issue Date Apr-2014
Publisher scopus
Journal Egyptian Journal of Neurology, Psychiatry and Neurosurgery 
URI http://research.asu.edu.eg/handle/123456789/2376


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