Peggy M Randon, Johann E Gudjonsson, Nicole L Ward
{"title":"关于银屑病关节炎,老鼠教会了我们什么?","authors":"Peggy M Randon, Johann E Gudjonsson, Nicole L Ward","doi":"10.1097/BOR.0000000000001093","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose of review: </strong>This review summarizes important mouse models of psoriatic arthritis (PsA), shedding light on their advantages and disadvantages in modeling human disease.</p><p><strong>Recent findings: </strong>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.</p><p><strong>Summary: </strong>Mouse models of PsA are powerful research tools for elucidating pathogenesis of disease, biomarker identification and may assist in the discovery of a cure.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"243-253"},"PeriodicalIF":4.3000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119223/pdf/","citationCount":"0","resultStr":"{\"title\":\"What are mice teaching us about psoriatic arthritis?\",\"authors\":\"Peggy M Randon, Johann E Gudjonsson, Nicole L Ward\",\"doi\":\"10.1097/BOR.0000000000001093\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose of review: </strong>This review summarizes important mouse models of psoriatic arthritis (PsA), shedding light on their advantages and disadvantages in modeling human disease.</p><p><strong>Recent findings: </strong>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.</p><p><strong>Summary: </strong>Mouse models of PsA are powerful research tools for elucidating pathogenesis of disease, biomarker identification and may assist in the discovery of a cure.</p>\",\"PeriodicalId\":11145,\"journal\":{\"name\":\"Current opinion in rheumatology\",\"volume\":\" \",\"pages\":\"243-253\"},\"PeriodicalIF\":4.3000,\"publicationDate\":\"2025-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119223/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current opinion in rheumatology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1097/BOR.0000000000001093\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/4/24 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"RHEUMATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current opinion in rheumatology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/BOR.0000000000001093","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/24 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"RHEUMATOLOGY","Score":null,"Total":0}
What are mice teaching us about psoriatic arthritis?
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.
期刊介绍:
A high impact review journal which boasts an international readership, Current Opinion in Rheumatology offers a broad-based perspective on the most recent and exciting developments within the field of rheumatology. Published bimonthly, each issue features insightful editorials and high quality invited reviews covering two or three key disciplines which include vasculitis syndromes, medical physiology and rheumatic diseases, crystal deposition diseases and rheumatoid arthritis. Each discipline introduces world renowned guest editors to ensure the journal is at the forefront of knowledge development and delivers balanced, expert assessments of advances from the previous year.