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Greve, B., Weissert, R., Hamdi, N., Bettelli, E., Sobel, R.A., Coyle, A., Kuchroo, V.K., Rajewsky, K. and Schmidt-Supprian, M. (2007) IκB Kinase 2/β Deficiency Controls Expansion of Autoreactive T Cells and Suppresses Experimental Autoimmune Encephalomyelitis. Journal of Immunology, 179, 179-185.
https://doi.org/10.4049/jimmunol.179.1.179

has been cited by the following article:

• TITLE: JAK-STAT Lodges in Multiple Sclerosis: Pathophysiology and Therapeutic Approach Overview

  AUTHORS: Kabir Magaji Hamid, Abdullahi Isiyaku, Mustapha Umar Kalgo, Isah Suleiman Yahaya, Abbas Mirshafiey

  KEYWORDS: Cytokines, Janus Kinases, Multiple Sclerosis, Neurogenesis, Signal Transduction, Transcription Factors

  JOURNAL NAME: Open Access Library Journal, Vol.4 No.4, April 27, 2017

  ABSTRACT: Multiple sclerosis (MS) is a complex inflammatory and demyelinating disease of central nervous system (CNS). The disease pathogenesis is not fully understood and no actual cure for the disease yet. The disease has genetic and environmental cause as fundamental factors which are identified for the disease pathogenesis so far. One of the characteristic features of the disease is inflammation cause due to activation of pro-inflammatory cells. Interference in signalling pathways such as JAK/STAT could result in physiological or pathological outcome in MS. Dysregulation of JAK/STAT signalling pathway is associated with chronic inflammatory process and immune disorders. In this review, considering the important role of JAK/STAT pathway in signal transduction of inflammatory process and immune responses in CNS, we describe the involvement of this signal transduction pathway in MS. Moreover, we consider the physiological and pathological involvement of JAK/STAT rout in neurogenesis/gliogenesis, cytokines production and as therapeutics target for managing MS.