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CARD9 in the pathogenesis of axial spondyloarthritis.
Seufert, A L; Struthers, H; Caplan, L; Napier, R J.
Afiliação
  • Seufert AL; Department of Molecular Microbiology and Immunology, Oregon Health & Science University, Portland, OR, USA. Electronic address: seufert@ohsu.edu.
  • Struthers H; Department of Molecular Microbiology and Immunology, Oregon Health & Science University, Portland, OR, USA. Electronic address: strutheh@ohsu.edu.
  • Caplan L; Rocky Mountain Regional VA Medical Center, Aurora, CO, 80045, USA. Electronic address: liron.caplan@cuanschutz.edu.
  • Napier RJ; Department of Molecular Microbiology and Immunology, Oregon Health & Science University, Portland, OR, USA; Division of Arthritis and Rheumatic Diseases, Oregon Health & Science University, USA; VA Portland Health Care System, Portland, OR, 97239, USA. Electronic address: napier@ohsu.edu.
Best Pract Res Clin Rheumatol ; : 101964, 2024 Jun 18.
Article em En | MEDLINE | ID: mdl-38897880
ABSTRACT
Axial spondyloarthritis (axSpA) has been long classified as an autoimmune disease caused by a breakdown in the ability of the immune system to delineate self from foreign, resulting in self-reactive T cells. The strong genetic association of HLA-B27 supports this role for T cells. More recently, genetic and clinical studies indicate a prominent role of the environment in triggering axSpA, including an important role for microbes and the innate immune response. As an example, mutations in genes associated with innate immunity, including the anti-fungal signaling molecule Caspase recruitment domain-containing protein 9 (CARD9), have been linked to axSpA susceptibility. Thus, current thought classifies axSpA as a "mixed pattern condition" caused by both autoimmune and autoinflammatory mechanisms. The goal of this review is to convey.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article