TY - JOUR
T1 - The IL-23/IL-17 axis in psoriatic arthritis
AU - Suzuki, Erika
AU - Mellins, Elizabeth D.
AU - Gershwin, M. Eric
AU - Nestle, Frank O.
AU - Adamopoulos, Iannis E.
N1 - Funding Information:
We thank Thanh Nguyen for the help with graphic design. Research reported in this publication was partly supported by the NIAMS/NIH AR62173 and Shriners Hospitals for Children SHC 250862 to IEA. ES is the recipient of a NCATS/NIH # UR1 TR000002 pre-doctoral fellowship. EDM is partly supported by NIH R01AR061297 . FON is partly supported by: EU FP7 grant agreement HEALTH-F2-2011-261366 and the National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London . The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH, SHC, NHS, NIHR or the Department of Health. We apologize to our colleagues for omissions imposed by space limitations.
PY - 2014/4
Y1 - 2014/4
N2 - Psoriatic arthritis (PsA) is an immune-mediated chronic inflammatory disease, affecting both the skin and joints. Disease progression is associated with aberrant cytokine expression, and TNF blockade is the most successful therapy to date. However, not all patients are responsive to anti-TNF treatment, highlighting the need to better understand the cellular and molecular mechanisms that govern the disease. PsA associations with single nucleotide polymorphisms in IL23R as well as TRAF3IP2 (Act1), a molecule downstream of the IL-17 receptor (IL-17R), have linked the IL-23/IL-17 axis to disease pathology. Although both cytokines are implicated in PsA, a full picture of their cellular targets and pathogenic mechanisms has not yet emerged. In this review, we focus on the IL-23/IL-17 axis-elicited responses mediated by osteoclasts, keratinocytes and neutrophils. Expanding our understanding of the cellular and molecular mechanisms that dictate pathogenicity in PsA will contribute to developing novel treatment strategies to combat disease.
AB - Psoriatic arthritis (PsA) is an immune-mediated chronic inflammatory disease, affecting both the skin and joints. Disease progression is associated with aberrant cytokine expression, and TNF blockade is the most successful therapy to date. However, not all patients are responsive to anti-TNF treatment, highlighting the need to better understand the cellular and molecular mechanisms that govern the disease. PsA associations with single nucleotide polymorphisms in IL23R as well as TRAF3IP2 (Act1), a molecule downstream of the IL-17 receptor (IL-17R), have linked the IL-23/IL-17 axis to disease pathology. Although both cytokines are implicated in PsA, a full picture of their cellular targets and pathogenic mechanisms has not yet emerged. In this review, we focus on the IL-23/IL-17 axis-elicited responses mediated by osteoclasts, keratinocytes and neutrophils. Expanding our understanding of the cellular and molecular mechanisms that dictate pathogenicity in PsA will contribute to developing novel treatment strategies to combat disease.
KW - IL-17
KW - IL-23
KW - NF-κB
KW - Psoriatic arthritis
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U2 - 10.1016/j.autrev.2014.01.050
DO - 10.1016/j.autrev.2014.01.050
M3 - Review article
C2 - 24424175
AN - SCOPUS:84896313565
SN - 1568-9972
VL - 13
SP - 496
EP - 502
JO - Autoimmunity Reviews
JF - Autoimmunity Reviews
IS - 4-5
ER -