Silencing of B cell activation factor gene and its implication in treating autoimmune arthritis

2007 ◽  
Author(s):  
Yan-kai Lin
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
Autoimmune Arthritis ◽  
B Cell Activation ◽  
Factor Gene ◽  
Activation Factor

scholarly journals B cell activation factor (BAFF) is a novel adipokine that links obesity and inflammation

2009 ◽  
Vol 41 (3) ◽  
pp. 208 ◽  
Author(s):  
Yu-Hee Kim ◽  
Bong-Hyuk Choi ◽  
Hyae-Gyeong Cheon ◽  
Myoung-Sool Do
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
B Cell Activation ◽  
Activation Factor

Blood stage Plasmodium falciparum antigens induce T cell independent immunoglobulin production via B cell activation factor of the TNF family (BAFF) pathway

Acta Tropica ◽  
2010 ◽  
Vol 116 (3) ◽  
pp. 217-226 ◽  
Author(s):  
Ratchanok Kumsiri ◽  
Pachuen Potup ◽  
Kesinee Chotivanich ◽  
Songsak Petmitr ◽  
Thareerat Kalambaheti ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
T Cell ◽  
B Cell ◽  
Cell Activation ◽  
Blood Stage ◽  
B Cell Activation ◽  
Immunoglobulin Production ◽  
Activation Factor

scholarly journals Ameliorated Autoimmune Arthritis and Impaired B Cell Receptor-Mediated Ca2+ Influx in Nkx2-3 Knock-out Mice

2020 ◽  
Vol 21 (17) ◽  
pp. 6162
Author(s):  
Esam Khanfar ◽  
Katalin Olasz ◽  
Fanni Gábris ◽  
Erzsébet Gajdócsi ◽  
Bálint Botz ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Clinical Picture ◽  
Cell Activation ◽  
Cell Receptor ◽  
Histological Structure ◽  
Autoimmune Arthritis ◽  
B Cell Activation ◽  
Knock Out ◽  
Radiological Changes

B cells play a crucial role in the pathogenesis of rheumatoid arthritis. In Nkx2-3-deficient mice (Nkx2-3−/−) the spleen’s histological structure is fundamentally changed; therefore, B cell homeostasis is seriously disturbed. Based on this, we were curious, whether autoimmune arthritis could be induced in Nkx2-3−/− mice and how B cell activation and function were affected. We induced arthritis with immunization of recombinant human proteoglycan aggrecan G1 domain in Nkx2-3−/− and control BALB/c mice. We followed the clinical picture, characterized the radiological changes, the immune response, and intracellular Ca2+ signaling of B cells. Incidence of the autoimmune arthritis was lower, and the disease severity was milder in Nkx2-3−/− mice than in control BALB/c mice. The radiological changes were in line with the clinical picture. In Nkx2-3−/− mice, we measured decreased antigen-induced proliferation and cytokine production in spleen cell cultures; in the sera, we found less anti-CCP-IgG2a, IL-17 and IFNγ, but more IL-1β, IL-4 and IL-6. B cells isolated from the lymph nodes of Nkx2-3−/− mice showed decreased intracellular Ca2+ signaling compared to those isolated from BALB/c mice. Our findings show that the transcription factor Nkx2-3 might regulate the development of autoimmune arthritis most likely through modifying B cell activation.

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