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.