On the other hand, positive correlations between serum levels of anti-Hsp60 IgG and IL-4 (Th2-like cytokine) or between serum levels of anti-Hsp90 IgG and IFN-ɣ (Th1-like cytokine) were found to be statistically significant in RA.
Moreover, MA could effectively stimulate the innate immune cytokines (IL-1[Formula: see text], IL-1[Formula: see text], IL-6, IL-7, IL-18, TNF-[Formula: see text]) and adaptive immunity cytokines (IL-2, IL-12, IFN-[Formula: see text], IL-4, IL-5, IL-10, IL-13, IL-17) as the main part of the immune response and repaired damage of RA.
Cluster analysis identified a specific B-cell factors profile overrepresented in RA and associated with autoantibodies, elevated proinflammatory cytokines (IFNα, MIP1α, TNFα, IL-37, and GM-CSF) and increased type-I IFN signature.
Combined occurrence of <i>PTPN2:rs478582</i> and <i>PTPN22:rs2476601</i> in association with the presence of MAP has significantly increased T-cell response and elevated <i>IFN-</i>γ expression in RA samples.
To validate the IFN response gene (IRG) set for the prediction of non-response to rituximab in rheumatoid arthritis (RA) and assess the predictive performance upon combination of this gene set with clinical parameters.
We observed that the expression of G<i>α</i>q was negatively correlated with the expression of signature Th1 cytokine (IFN-<i>γ</i>) in RA patients, which suggests a negative role of G<i>α</i>q in differentiation of Th1 cells.
Increased expression of type I IFN genes, also referred to as an IFN signature, has been detected in various autoimmune diseases including rheumatoid arthritis (RA).
This study was designed to investigate the role of the IKK-related kinase IKKepsilon and IFN regulatory factor 3 (IRF-3) in the activation of antiviral genes in rheumatoid arthritis (RA).
As well, the ability of IFN-a to regulate gene expression levels for osteoprotegerin (OPG) and osteoprotegerin ligand (OPGL) was examined in freshly isolated SF cells from patients with RA, by reverse transcriptase polymerase chain reaction.