Next Article in Journal
Hsp60 in Skeletal Muscle Fiber Biogenesis and Homeostasis: From Physical Exercise to Skeletal Muscle Pathology
Previous Article in Journal
Lack of LTβR Increases Susceptibility of IPEC-J2 Cells to Porcine Epidemic Diarrhea Virus
Article Menu

Export Article

Open AccessReview
Cells 2018, 7(12), 223;

Defective T-Cell Apoptosis and T-Regulatory Cell Dysfunction in Rheumatoid Arthritis

Department of Medicine, Division of Rheumatic Diseases, Case Western Reserve University School of Medicine, Foley Medical Building, 2061 Cornell Road, Suite 207, Cleveland, OH 44122-5076, USA
Department of Medicine, University Hospitals Cleveland Medical Center, Cleveland, OH 44106, USA
Received: 16 October 2018 / Revised: 13 November 2018 / Accepted: 20 November 2018 / Published: 22 November 2018
(This article belongs to the Special Issue The Molecular and Cellular Basis for Rheumatoid Arthritis)
Full-Text   |   PDF [237 KB, uploaded 22 November 2018]


Rheumatoid arthritis (RA) is a chronic, progressive, systemic autoimmune disease that mostly affects small and large synovial joints. At the molecular level, RA is characterized by a profoundly defective innate and adaptive immune response that results in a chronic state of inflammation. Two of the most significant alterations in T-lymphocyte (T-cell) dysfunction in RA is the perpetual activation of T-cells that result in an abnormal proliferation state which also stimulate the proliferation of fibroblasts within the joint synovial tissue. This event results in what we have termed “apoptosis resistance”, which we believe is the leading cause of aberrant cell survival in RA. Finding therapies that will induce apoptosis under these conditions is one of the current goals of drug discovery. Over the past several years, a number of T-cell subsets have been identified. One of these T-cell subsets are the T-regulatory (Treg) cells. Under normal conditions Treg cells dictate the state of immune tolerance. However, in RA, the function of Treg cells become compromised resulting in Treg cell dysfunction. It has now been shown that several of the drugs employed in the medical therapy of RA can partially restore Treg cell function, which has also been associated with amelioration of the clinical symptoms of RA. View Full-Text
Keywords: apoptosis; inflammation; T-lymphocytes; rheumatoid arthritis; synovial fibroblasts apoptosis; inflammation; T-lymphocytes; rheumatoid arthritis; synovial fibroblasts
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Malemud, C.J. Defective T-Cell Apoptosis and T-Regulatory Cell Dysfunction in Rheumatoid Arthritis. Cells 2018, 7, 223.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Cells EISSN 2073-4409 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top