TY - JOUR
T1 - IL-17 Inhibition in Axial Spondyloarthritis
AU - Danve, Abhijeet
AU - Deodhar, Atul
N1 - Funding Information:
Atul Deodhar reports grants from Amgen, AbbVie, Janssen, Novartis, Pfizer, and UCB and personal fees from Amgen, AbbVie, Janssen, Novartis, Pfizer, and UCB, outside the submitted work, and Dr. Deodhar has received research grants to conduct studies on secukinumab, a drug described in the manuscript. He is also an author on the published studies on secukinumab and has served on the Advisory Boards for Novartis, the company that owns the drug.
Publisher Copyright:
© 2015, Springer International Publishing AG.
PY - 2015/6/1
Y1 - 2015/6/1
N2 - Axial spondyloarthritis (axSpA) affects 0.5–1.5 % of western population. Although TNF inhibitor (TNFi) medications have dramatically improved the treatment of this disabling disease, there are almost 40 % of patients who do not respond or have intolerance to TNFi. Several genetic, animal model, translational, and clinical studies have confirmed the role of IL-23/IL-17 pathway in the pathogenesis of the axSpA. This axis could be targeted upstream by inhibiting either IL-23 or IL-23 receptor (IL-23R) or downstream by blocking IL-17 or IL-1RA receptor. Ustekinumab, a monoclonal antibody against p40 subunit of IL-12 and IL-23, and secukinumab, a monoclonal antibody against IL-17, have both demonstrated significant beneficial effect in controlling the disease activity, quality of life, and physical function as well as MRI scores in axSpA. Combined IL-17 and TNF-α blockade is a novel option for the patients with axSpA, which needs to be investigated further. We need prospective trials to evaluate the effect of IL-23/IL-17 axis manipulation on the radiographic progression and also on the extra-articular manifestations of axSpA.
AB - Axial spondyloarthritis (axSpA) affects 0.5–1.5 % of western population. Although TNF inhibitor (TNFi) medications have dramatically improved the treatment of this disabling disease, there are almost 40 % of patients who do not respond or have intolerance to TNFi. Several genetic, animal model, translational, and clinical studies have confirmed the role of IL-23/IL-17 pathway in the pathogenesis of the axSpA. This axis could be targeted upstream by inhibiting either IL-23 or IL-23 receptor (IL-23R) or downstream by blocking IL-17 or IL-1RA receptor. Ustekinumab, a monoclonal antibody against p40 subunit of IL-12 and IL-23, and secukinumab, a monoclonal antibody against IL-17, have both demonstrated significant beneficial effect in controlling the disease activity, quality of life, and physical function as well as MRI scores in axSpA. Combined IL-17 and TNF-α blockade is a novel option for the patients with axSpA, which needs to be investigated further. We need prospective trials to evaluate the effect of IL-23/IL-17 axis manipulation on the radiographic progression and also on the extra-articular manifestations of axSpA.
KW - Ankylosing spondylitis
KW - Axial spondyloarthritis
KW - Interleukin-17
KW - Interleukin-17 inhibitors
KW - Interleukin-23
KW - Secukinumab
KW - Th17 cells
KW - Ustekinumab
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U2 - 10.1007/s40674-015-0020-9
DO - 10.1007/s40674-015-0020-9
M3 - Review article
AN - SCOPUS:85043550754
SN - 2198-6002
VL - 1
SP - 221
EP - 230
JO - Current Treatment Options in Rheumatology
JF - Current Treatment Options in Rheumatology
IS - 2
ER -