Iain McInnes: Difference between revisions

McInnes's research has investigated the role of cytokines and their inflammation amplification role in immune-mediated inflammatory disease (IMID) pathogenesis. His early work focused on defining the roles played by novel cytokines in driving inflammatory synovitis, including the effector functions of IL-15, IL-18, and IL-33 in rheumatoid (RA) and psoriatic arthritis (PsA) synovitis.<ref name="il15">{{cite journal | url=https://pubmed.ncbi.nlm.nih.gov/9018238/ | pmid=9018238 | date=1997 | last1=McInnes | first1=I. B. | last2=Leung | first2=B. P. | last3=Sturrock | first3=R. D. | last4=Field | first4=M. | last5=Liew | first5=F. Y. | title=Interleukin-15 mediates T cell-dependent regulation of tumor necrosis factor-alpha production in rheumatoid arthritis | journal=Nature Medicine | volume=3 | issue=2 | pages=189–195 | doi=10.1038/nm0297-189 }}</ref><ref name="il18">{{cite journal | pmid=10562301 | date=1999 | last1=Gracie | first1=J. A. | last2=Forsey | first2=R. J. | last3=Chan | first3=W. L. | last4=Gilmour | first4=A. | last5=Leung | first5=B. P. | last6=Greer | first6=M. R. | last7=Kennedy | first7=K. | last8=Carter | first8=R. | last9=Wei | first9=X. Q. | last10=Xu | first10=D. | last11=Field | first11=M. | last12=Foulis | first12=A. | last13=Liew | first13=F. Y. | last14=McInnes | first14=I. B. | title=A proinflammatory role for IL-18 in rheumatoid arthritis | journal=The Journal of Clinical Investigation | volume=104 | issue=10 | pages=1393–1701 | doi=10.1172/JCI7317 | pmc=409841 }}</ref><ref name="il33">{{cite journal | url=https://pubmed.ncbi.nlm.nih.gov/20139274/ | pmid=20139274 | date=2010 | last1=Xu | first1=D. | last2=Jiang | first2=H. R. | last3=Li | first3=Y. | last4=Pushparaj | first4=P. N. | last5=Kurowska-Stolarska | first5=M. | last6=Leung | first6=B. P. | last7=Mu | first7=R. | last8=Tay | first8=H. K. | last9=McKenzie | first9=A. N. | last10=McInnes | first10=I. B. | last11=Melendez | first11=A. J. | last12=Liew | first12=F. Y. | title=IL-33 exacerbates autoantibody-induced arthritis | journal=Journal of Immunology (Baltimore, Md. : 1950) | volume=184 | issue=5 | pages=2620–2626 | doi=10.4049/jimmunol.0902685 }}</ref> His studies also examined the cytokine-driven cellular interactions between T cells, macrophages, and synovial fibroblasts, particularly the role of non-antigen dependent amplification of synovial inflammation.<ref name="synovial1">{{cite journal | pmid=11094451 | date=2000 | last1=McInnes | first1=I. B. | last2=Leung | first2=B. P. | last3=Liew | first3=F. Y. | title=Cell-cell interactions in synovitis. Interactions between T lymphocytes and synovial cells | journal=Arthritis Research | volume=2 | issue=5 | pages=374–378 | doi=10.1186/ar115 | doi-access=free | pmc=130139 }}</ref><ref name="synovial2">{{cite journal | url=https://www.nature.com/articles/nri2094#:~:text=Cytokines%20are%20implicated%20in%20each,destruction%20of%20adjacent%20joint%20tissue | doi=10.1038/nri2094 | title=Cytokines in the pathogenesis of rheumatoid arthritis | date=2007 | last1=McInnes | first1=Iain B. | last2=Schett | first2=Georg | journal=Nature Reviews Immunology | volume=7 | issue=6 | pages=429–442 | pmid=17525752 }}</ref>