Nevertheless, continued growth of RA contributions may overwhelm vulnerable age groups such as young adults.
This finding was confirmed when we performed correlation analyses of observed annual changes in d y, Δ A and Δ Y with observed increases in RA contributions of young adults ∆ aY.
While adaptive immunity plays a key role in the pathogenesis of RA, the contribution of innate immune responses has been increasingly appreciated in recent years.
This may argue that, in human RA, the contribution of IL-1 is overruled, or dominant pathways besides autoimmune IC- and T cell-driven processes play a role and have yet to be identified.
A study by Popa et al. [ 70] demonstrated the existence of an inverse correlation between severity of inflammation and circulating leptin levels in active RA, suggesting contribution of chronic inflammation to lowering plasma leptin concentration.
Other conditions associated with chronically elevated levels of inflammatory cytokines (e.g., aging, chronic kidney disease, obesity) are also associated with an increased prevalence of CHF [ 121, 70]; however, as in RA, the contributions of various non-inflammatory confounders in each of these conditions to the pathogenesis of CHF have not been fully explored.
In this review, we will explore the different animal models of RA, and their contribution to elucidating the role that effector T cells play in the regulation, induction, and maintenance of inflammatory joint disease.
However, while the rheumatologic and scientific community is in all probability now quite familiar with angiogenesis and its role in RA pathogenesis, the contribution made by EPC to blood vessel formation is less well understood.
Contribution: RA and JML designed research; SG and RB carried out the molecular genetic studies; RA, JML, AGS, CJ, EM, and CR analyzed and interpreted data; RA designed, performed, and wrote the manuscript; JML supervised the research and critically revised the manuscript.
Contribution: RA, JML and CR designed research; RA and RB performed molecular and functional experiments; RA, JML, TC, RB, CJ, EM, and CR analyzed and interpreted data; RA designed, performed, and wrote the manuscript; JML and CR supervised the research and critically revised the manuscript.
This issue of Arthritis Research and Therapy contains a succinct and elegant paper by Michou and colleagues that advances our understanding of the genetic basis of rheumatoid arthritis (RA) by reclassifying the contribution of RA susceptibility alleles according to their structure.
