Effect of gold therapy on CD5+ B-cells and TCR ?? + T-cells in patients with rheumatoid arthritis

1991 ◽  
Vol 11 (4-5) ◽  
pp. 175-178 ◽  
Author(s):  
J. Hassan ◽  
C. Feighery ◽  
B. Bresnihan ◽  
A. Whelan
10.1186/ar128 ◽  
2000 ◽  
Vol 2 (6) ◽  
Author(s):  
Cornelia M Weyand ◽  
Jörg J Goronzy ◽  
Seisuke Takemura ◽  
Paul J Kurtin

2014 ◽  
Vol 1 (1) ◽  
pp. 34-37
Author(s):  
Khalid Testas ◽  
◽  
Samy Slimani ◽  
Lamia Djeghader ◽  

Remission of low disease activity has become the main goal in the management of rheumatoid arthritis (RA), thanks to immunosuppressants but more importantly to a new emerging drug called biologics. Biologics used in RA have proved their efficacy on symptoms as well as radiographic progression, and they have been integrated into the recommendations for the management of RA. TNF alpha inhibitors with their five different molecules are the most prescribed bDMARDs in the world since their approval during the 1990s. Since then, more molecules were made available, targeting other compounds of the rheumatoid inflammation: IL1 (Anakinra), CD20 B cells (Rituximab), costimulation molecules of T cells (Abatacept), IL6 (Tocilizumab) and more recently small molecule inhibitors (Janus kinases), Tofacitinib.


2018 ◽  
Vol 9 ◽  
Author(s):  
Julie Mielle ◽  
Rachel Audo ◽  
Michael Hahne ◽  
Laurence Macia ◽  
Bernard Combe ◽  
...  

2021 ◽  
Author(s):  
Dornatien C Anang ◽  
Tamara H. Ramwadhdoebe ◽  
Janine Hahnlein ◽  
Bo van Kuijk ◽  
Noortje Smits ◽  
...  

Objectives: Follicular helper T cells (Tfh cells) provide key B cell help, and are essential in germinal center (GC) formation and (auto) antibody generation. To gain more insight into their role during the earliest phase of rheumatoid arthritis (RA) we analyzed their frequencies, phenotype and cytokine profile in peripheral blood and lymphoid tissues. Methods: Using flow cytometry, we studied the frequency of Tfh and B cells in peripheral blood and lymph node (LN) needle biopsies. Three donor groups were included and compared: healthy controls (HCs), autoantibody positive individuals at risk for developing RA (RA-risk individuals), and early RA patients. Ex vivo stimulation of lymphocytes with PMA/ionomycin was performed to assess cytokine secretion by Tfh cells. Results: In blood, the frequency of circular Tfh cells (cTfh) did not differ between study groups. In lymphoid tissue, the frequency of Tfh cells correlated strongly with the frequency of CD19+ B cells. Compared to healthy controls, LN samples of RA patients and RA-risk individuals showed more CD19+ B cells and more CD4+CXCR5+ and CD8+CXCR5+ Tfh cells. These Tfh cells from LNs expressed less IL-21 upon ex vivo stimulation. Conclusion: LN tissue of early RA patients as well as part of RA-risk individuals exhibit increased frequencies of Tfh cells correlating with increased numbers of B cells. Interestingly, IL-21 production is already aberrant in the very early at risk phase of the disease. This suggests that Tfh cells may present a novel rationale for therapeutic targeting during the preclinical stage of the disease to prevent further disease progression.


2013 ◽  
Vol 74 (1) ◽  
pp. 294-302 ◽  
Author(s):  
Laetitia Rapetti ◽  
Konstantia-Maria Chavele ◽  
Catherine M Evans ◽  
Michael R Ehrenstein

ObjectiveTo investigate whether regulatory T cells (Treg) can control B cell function in rheumatoid arthritis (RA) and if not to explore the basis for this defect.MethodsSuppression of B cell responses by Treg was analysed in vitro by flow cytometry and ELISA using peripheral blood mononuclear cells from 65 patients with RA and 41 sex-matched and aged-matched healthy volunteers. Blocking and agonistic antibodies were used to define the role of Fas-mediated apoptosis in B cell regulation.ResultsTreg failed to restrain B cell activation, proinflammatory cytokine and antibody production in the presence of responder T cells in RA patients. This lack of suppression was not only caused by impaired Treg function but was also due to B cell resistance to regulation. In healthy donors, control by Treg was associated with increased B cell death and relied upon Fas-mediated apoptosis. In contrast, RA B cells had reduced Fas expression compared with their healthy counterparts and were resistant to Fas-mediated apoptosis.ConclusionsThese studies demonstrate that Treg are unable to limit B cell responses in RA. This appears to be primarily due to B cell resistance to suppression, but Treg defects also contribute to this failure of regulation. Our data identify the Fas pathway as a novel target for Treg-mediated suppression of B cells and highlight a potential therapeutic approach to restore control of B cells by Treg in RA patients.


1992 ◽  
pp. 122-136
Author(s):  
C. Plater-Zyberk ◽  
R. N. Maini ◽  
F. M. Brennan ◽  
M. Feldmann

2021 ◽  
Vol 360 ◽  
pp. 104263
Author(s):  
Tsuyoshi Nakayama ◽  
Motoki Yoshimura ◽  
Kazuhiko Higashioka ◽  
Kohta Miyawaki ◽  
Yuri Ota ◽  
...  

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