alexa Intracellular Signaling Pathways in Rheumatoid Arthritis | OMICS International | Abstract
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Review Article

Intracellular Signaling Pathways in Rheumatoid Arthritis

Charles J Malemud*
Arthritis Research Laboratory, Department of Medicine, Division of Rheumatic Diseases, Case Western Reserve University, School of Medicine and University Hospitals Case Medical Center, Cleveland, Ohio 44106, USA
Corresponding Author : Charles J. Malemud, Ph.D.
Department of Medicine, Division of Rheumatic Diseases
University Hospitals Case Medical Center
Foley Medical Building, 2061 Cornell Road
Rm. 207, Cleveland, Ohio 44106-5076 USA
Tel: (216) 844-7846
Fax: (216) 844-2288
E-mail: [email protected]
Received: June 12, 2013; Accepted: August 13, 2013; Published: August 19, 2013
Citation: Malemud CJ (2013) Intracellular Signaling Pathways in Rheumatoid Arthritis. J Clin Cell Immunol 4:160. doi:10.4172/2155-9899.1000160
Copyright: © 2013 Malemud CJ. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Dysfunctional intracellular signaling involving deregulated activation of the Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) and “cross-talk” between JAK/STAT and the stress-activated protein kinase/mitogen-activated protein kinase (SAPK/MAPK) and Phosphatidylinositide-3-Kinase/AKT/mammalian Target of Rapamycin (PI-3K/AKT/mTOR) pathways play a critical role in rheumatoid arthritis. This is exemplified by immune-mediated chronic inflammation, up-regulated matrix metalloproteinase gene expression, induction of articular chondrocyte apoptosis and “apoptosis-resistance” in rheumatoid synovial tissue. An important consideration in the development of novel therapeutics for rheumatoid arthritis will be the extent to which inhibiting these signal transduction pathways will sufficiently suppress immune cell-mediated inflammation to produce a lasting clinical remission and halt the progression of rheumatoid arthritis pathology. In that regard, the majority of the evidence accumulated over the past decade indicated that merely suppressing pro-inflammatory cytokine-mediated JAK/ STAT, SAPK/MAPK or PI-3K/AKT/mTOR activation in RA patients may be necessary but not sufficient to result in clinical improvement. Thus, targeting aberrant enzyme activities of spleen tyrosine kinase, sphingosine kinases-1, -2, transforming growth factor β-activated kinase-1, bone marrow kinase, and nuclear factor-κB-inducing kinase for intervention may also have to be considered.

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