Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 496-502 |
| Number of pages | 7 |
| Journal | Autoimmunity Reviews |
| Volume | 13 |
| Issue number | 4-5 |
| DOIs | |
| State | Published - 2014 |
Fingerprint
Keywords
- IL-17
- IL-23
- NF-κB
- Psoriatic arthritis
ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
Cite this
The IL-23/IL-17 axis in psoriatic arthritis. / Suzuki, Erika; Mellins, Elizabeth D.; Gershwin, M. Eric; Nestle, Frank O.; Adamopoulos, Iannis.
In: Autoimmunity Reviews, Vol. 13, No. 4-5, 2014, p. 496-502.Research output: Contribution to journal › Article
}
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
PY - 2014
Y1 - 2014
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
UR - http://www.scopus.com/inward/record.url?scp=84896313565&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84896313565&partnerID=8YFLogxK
U2 - 10.1016/j.autrev.2014.01.050
DO - 10.1016/j.autrev.2014.01.050
M3 - Article
C2 - 24424175
AN - SCOPUS:84896313565
VL - 13
SP - 496
EP - 502
JO - Autoimmunity Reviews
JF - Autoimmunity Reviews
SN - 1568-9972
IS - 4-5
ER -