Cytokines in the pathogenesis of rheumatoid arthritis

By I. McInnes, Georg Schett. Nature reviews. Immunology, 2007

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Immunopathogenesis of rheumatoid arthritis (2017, positive): “…non-antigen-dependent manner, the cytokine-rich synovial milieu, particularly IL-15, IL-7, and IL-6, can induce integrin and Ig-superfamilydependent interactions between CD45RO+ memory T cells and macrophages to drive subsequent macrophage cytokine and chemokine release (McInnes and Schett, 2007).”
Colony-stimulating factors in inflammation and autoimmunity (2008, background): “Therapeutic implications of targeting CSFs Clinical trials involving GM-CSF and M-CSF blockade have recently commenced in patients with rheumatoid arthritis ( Table 1 ), although there seems to be limited awareness generally of the potential relevance of the CSFs to its pathogenesi”
Therapeutic strategies for the clinical blockade of IL-6/gp130 signaling. (2011, background): “However, cytokines that signal via this pathway (e.g., IFN-γ , GM-CSF, IL-6, IL-10, IL-15, IL-23) have become increasingly linked with the pathogenesis of chronic inflammatory diseases and cancer (2, 4).”
Structure and signalling in the IL-17 receptor superfamily (2009, positive): “For example, antibodies and soluble receptors that neutralize TNF have revolutionized the treatment of autoimmune disease”
Oral microbiomes: more and more importance in oral cavity and whole body (2018, background): “contribute to disease pathogenesis (McInnes and Schett, 2011; Raychaudhuri et al., 2012; Okada et al., 2014; McInnes and Schett, 2007; Viatte et al., 2013).”