scholarly journals Editorial: Quality or quantity? Unraveling the role of Treg cells in rheumatoid arthritis

2013 ◽  
Vol 65 (3) ◽  
pp. 552-554 ◽  
Author(s):  
Berent Prakken ◽  
Ellen Wehrens ◽  
Femke van Wijk
Keyword(s):  
Rheumatoid Arthritis ◽  
Treg Cells

scholarly journals Function and Role of Regulatory T Cells in Rheumatoid Arthritis

2021 ◽  
Vol 12 ◽  
Author(s):  
Qi Jiang ◽  
Guocan Yang ◽  
Qi Liu ◽  
Shengjun Wang ◽  
Dawei Cui
Keyword(s):  
Rheumatoid Arthritis ◽  
Autoimmune Diseases ◽  
Tissue Injury ◽  
Treg Cells ◽  
Self Tolerance ◽  
Progression Of Disease ◽  
Loss Of Tolerance ◽  
Vital Component ◽  
The Ideal

Rheumatoid arthritis (RA) is a systemic and heterogeneous autoimmune disease with symmetrical polyarthritis as its critical clinical manifestation. The basic cause of autoimmune diseases is the loss of tolerance to self or harmless antigens. The loss or functional deficiency of key immune cells, regulatory T (Treg) cells, has been confirmed in human autoimmune diseases. The pathogenesis of RA is complex, and the dysfunction of Tregs is one of the proposed mechanisms underlying the breakdown of self-tolerance leading to the progression of RA. Treg cells are a vital component of peripheral immune tolerance, and the transcription factor Foxp3 plays a major immunosuppressive role. Clinical treatment for RA mainly utilizes drugs to alleviate the progression of disease and relieve disease activity, and the ideal treatment strategy should be to re-induce self-tolerance before obvious tissue injury. Treg cells are one of the ideal options. This review will introduce the classification, mechanism of action, and characteristics of Treg cells in RA, which provides insights into clinical RA treatment.

A1.5 Rheumatoid arthritis alters the preservative role of IL-15 on bone-marrow-resident TREG cells towards a pro-inflammatory phenotype

2015 ◽  
Vol 74 (Suppl 1) ◽  
pp. A2.2-A2
Author(s):  
M Massalska ◽  
E Kuca-Warnawin ◽  
A Radzikowska ◽  
U Musialowicz ◽  
U Skalska ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Bone Marrow ◽  
Treg Cells ◽  
Inflammatory Phenotype

scholarly journals Altered Immunoregulation in Rheumatoid Arthritis: The Role of Regulatory T Cells and Proinflammatory Th17 Cells and Therapeutic Implications

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Alessia Alunno ◽  
Mirko Manetti ◽  
Sara Caterbi ◽  
Lidia Ibba-Manneschi ◽  
Onelia Bistoni ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Th17 Cells ◽  
Current Knowledge ◽  
Cell Subset ◽  
Treg Cells ◽  
Lymphocyte Subpopulations ◽  
Therapeutic Targeting ◽  
Therapeutic Implications ◽  
T Lymphocyte Subpopulations

In recent years several studies investigated the role of T lymphocyte subpopulations in the pathogenesis of rheumatoid arthritis (RA). Pathogenic Th17 cells mediate pannus growth, osteoclastogenesis, and synovial neoangiogenesis; hence they are key players in the development of the disease. On the other hand, regulatory T (Treg) cells are a T cell subset whose peculiar function is to suppress autoreactive lymphocytes. The imbalance between Th17 and Treg cells has been identified as a crucial event in the pathogenesis of RA. In addition, the effects of currently employed RA therapeutic strategies on these lymphocyte subpopulations have been extensively investigated. This review article aims to discuss current knowledge on Treg and Th17 cells in RA and possible implications of their therapeutic targeting in this disorder.

Role of Innate Immune Sensors, TLRs, and NALP3 in Rheumatoid Arthritis and Osteoarthritis

2014 ◽  
Vol 24 (4) ◽  
pp. 243-251 ◽  
Author(s):  
Yuya Takakubo ◽  
G. Barreto ◽  
Yrjo T. Konttinen ◽  
H. Oki ◽  
Michiaki Takagi
Keyword(s):  
Rheumatoid Arthritis ◽  
Innate Immune

Role of matrix metalloproteinase in the development of pericardial effusion in patients with rheumatoid arthritis

2018 ◽  
Vol 16 (7(part 2)) ◽  
pp. 99-101
Author(s):  
L. I. Feiskhanova ◽  
◽  
I. Kh. Valeeva ◽  
A. K. Feiskhanov ◽  
◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Pericardial Effusion ◽  
Matrix Metalloproteinase
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