What are mice teaching us about psoriatic arthritis?
Peggy M Randon1, Johann E Gudjonsson2, Nicole L Ward3,4
1Medical Scientist Training Program, Vanderbilt University School of Medicine, Nashville, Tennessee.
Purpose Of Review:
This review summarizes important mouse models of psoriatic arthritis (PsA), shedding light on their advantages and disadvantages in modeling human disease.
Recent Findings:
Two newly created mouse models of PsA validate NF-κB signaling as disease-causing and identify pathogenic roles for CD8 + and CD4 + FoxP3 + T cells in the development of specific PsA phenotypes. The IkbkbGoF/GoF model demonstrates that homozygosity for a gain-of-function mutation in Ikbkb results in expansion of FoxP3 + CD25 + IL-17A + Tregs that lead to the development of dactylitis, spondylitis and PsA-like changes to the nails and skin, and when transferred to wildtype mice, reproduce these outcomes. The humanized mouse PsA model (Hu-PsA) establishes that introduction of PsA patient sera and PBMCs into NSG-SGM3 mice has the capacity to elicit distinct subtypes of PsA and identifies a critical role for CD8 + IL-32 + CXCL14 + T cells and immunoglobulins in disease development.
Summary:
Mouse models of PsA are powerful research tools for elucidating pathogenesis of disease, biomarker identification and may assist in the discovery of a cure.
