Differential cytokine secretion results from p65 and c-Rel NF-κB subunit signaling in peripheral blood mononuclear cells of TNF receptor-associated periodic syndrome patients

2011 ◽  
Vol 268 (2) ◽  
pp. 55-59 ◽  
Author(s):  
Belinda Nedjai ◽  
Graham A. Hitman ◽  
Leigh D. Church ◽  
Kirsten Minden ◽  
Margo L. Whiteford ◽  
...  
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Cytokine Secretion ◽  
Periodic Syndrome ◽  
Tnf Receptor ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

scholarly journals Expression of TNF-αand Related Signaling Molecules in the Peripheral Blood Mononuclear Cells of Rheumatoid Arthritis Patients

2006 ◽  
Vol 2006 ◽  
pp. 1-5 ◽  
Author(s):  
Sunil Kumar Raghav ◽  
Bhawna Gupta ◽  
Charu Agrawal ◽  
Ved P. Chaturvedi ◽  
Hasi R. Das
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Constitutive Expression ◽  
Tnf Receptor ◽  
Death Domain ◽  
Peripheral Blood Mononuclear ◽  
Interacting Protein ◽  
Blood Mononuclear Cells ◽  
Domain Protein

We examined the role of tumor necrosis factor (TNF-α) and its related signaling intermediates leading to apoptosis/proliferation in the peripheral blood mononuclear cells (PBMCs) of RA patients. The constitutive expression of mRNA for TNF-αreceptors (TNFR-I and TNFR-II) and the adapter molecules, such as the TNF receptor-associated death domain protein (TRADD), Fas-associated death domain protein (FADD), receptor interacting protein (RIP), and TNF receptor-associated factor 2 (TRAF-2) were analyzed by reverse transcriptase-PCR (RT-PCR) in PBMCs from control and RA cases. PBMCs of RA patients showed a significant increase in TNF-αand TNFR-I expression as compared with that from control subjects along with significantly increased constitutive expression of TRADD, RIP, and TRAF-2 mRNA. There was a decrease in expression of FADD in RA patients, but the difference was not significant as compared to controls. These data suggested enhanced signaling by the TNFR-I-TRADD-RIP-TRAF-2 pathway and suppressed signaling by the TNFR-I-TRADD-FADD pathway in PBMCs of RA patients. However, the regulatory mechanisms for TNF-αinduced signaling may not be explained only by these pathways.

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