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Recent genetic advances in innate immunity of psoriatic arthritis
被引:14
|作者:
Hile, Grace
[1
]
Kahlenberg, J. Michelle
[2
]
Gudjonsson, Johann E.
[1
]
机构:
[1] Univ Michigan, Dept Dermatol, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Dept Internal Med, Div Rheumatol, Ann Arbor, MI 48109 USA
关键词:
GENOME-WIDE ASSOCIATION;
T-CELLS;
ANKYLOSING-SPONDYLITIS;
NEUTROPHIL RECRUITMENT;
RECEPTOR ACTIVATOR;
CHEMOKINE RELEASE;
IL-23/IL-17;
AXIS;
DENDRITIC CELLS;
CUTTING EDGE;
HLA-C;
D O I:
10.1016/j.clim.2020.108405
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Psoriatic arthritis (PsA) is a heterogeneous disease that affects multiple organ systems including the peripheral and axial joints, entheses and nails. PsA is associated with significant comorbidities including cardiovascular, metabolic, and psychiatric diseases. The pathogenesis of PsA is complex and involves genetic, immunologic and environmental factors. Recent evidence suggests the heritability for PsA to be stronger and distinct from that of PsC. Prominent genes identified via GWAS for PsA include HLA-B/C, HLA-B, IL12B, IL23R, TNP1, TRAF3IP3, and REL. We review the genetics of psoriatic arthritis and discuss the role of the innate immune system as important in the pathogenesis of PsA by focusing on key signaling pathways and cellular makeup. Understanding the candidate genes identified in PsA highlights pathways of critical importance to the pathogenesis of psoriatic disease including the key role of the innate immune response, mediated through IL-23/IL-17 axis, RANK and NF kappa B signaling pathways.
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