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2014 ; 13
(4-5
): 496-502
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The IL-23/IL-17 axis in psoriatic arthritis
#MMPMID24424175
Suzuki E
; Mellins ED
; Gershwin ME
; Nestle FO
; Adamopoulos IE
Autoimmun Rev
2014[Apr]; 13
(4-5
): 496-502
PMID24424175
show ga
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.
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