Arterial immune protein expression demonstrates the complexity of immune responses in Kawasaki disease arteritis.

Cameron, S A; White, S M; Arrollo, D; Shulman, S T; Rowley, A H

Cameron, S A; White, S M; Arrollo, D; Shulman, S T; Rowley, A H.

Afiliación

Cameron SA; Department of Pediatrics/Cardiology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
White SM; Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Arrollo D; Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Shulman ST; Pediatrics/Infectious Diseases, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, IL, USA.
Rowley AH; Northwestern University Feinberg School of Medicine, Chicago, IL, USA.

Clin Exp Immunol ; 190(2): 244-250, 2017 11.

Article en En | MEDLINE | ID: mdl-28707750

RESUMEN

A more complete understanding of immune-mediated damage to the coronary arteries in children with Kawasaki disease (KD) is required for improvements in patient treatment and outcomes. We recently reported the transcriptional profile of KD coronary arteritis, and in this study sought to determine protein expression of transcriptionally up-regulated immune genes in KD coronary arteries from the first 2 months after disease onset. We examined the coronary arteries of 12 fatal KD cases and 13 childhood controls for expression of a set of proteins whose genes were highly up-regulated in the KD coronary artery transcriptome: allograft inflammatory factor 1 (AIF1), interleukin 18 (IL-18), CD74, CD1c, CD20 (MS4A1), Toll-like receptor 7 (TLR-7) and Z-DNA binding protein 1 (ZBP1). Immunohistochemistry and immunofluorescence studies were performed to evaluate protein expression and co-localization, respectively. AIF1 was expressed transmurally in KD arteritis and localized to macrophages and myeloid dendritic cells. CD74, which interacts with major histocompatibility complex (MHC) class II on antigen-presenting cells, localized to the intima-media. CD1c, a marker of myeloid dendritic cells, was expressed in a transmural pattern, as were IL-18 and CD20. ZBP1 and TLR-7 were up-regulated compared to controls, but less highly compared to the other proteins. These findings provide evidence of antigen presentation and interferon response in KD arteritis. In combination with prior studies demonstrating T lymphocyte activation, these results demonstrate the complexity of the KD arterial immune response.

Asunto(s)

Arteritis/inmunología; Vasos Coronarios/inmunología; Expresión Génica; Síndrome Mucocutáneo Linfonodular/inmunología; Síndrome Mucocutáneo Linfonodular/metabolismo; Presentación de Antígeno; Antígenos CD/genética; Antígenos CD1/genética; Antígenos CD20/genética; Arteritis/fisiopatología; Proteínas de Unión al Calcio; Aneurisma Coronario/inmunología; Vasos Coronarios/fisiopatología; Proteínas de Unión al ADN/genética; Femenino; Técnica del Anticuerpo Fluorescente; Perfilación de la Expresión Génica; Glicoproteínas/genética; Humanos; Inmunohistoquímica; Lactante; Interleucina-18/genética; Masculino; Proteínas de Microfilamentos; Síndrome Mucocutáneo Linfonodular/complicaciones; Síndrome Mucocutáneo Linfonodular/mortalidad; Proteínas de Unión al ARN; Sialiltransferasas/genética; Receptor Toll-Like 7/genética

Palabras clave

AIF1; Kawasaki Diseas; coronary aneurysm

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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Arteritis / Expresión Génica / Vasos Coronarios / Síndrome Mucocutáneo Linfonodular Límite: Female / Humans / Infant / Male Idioma: En Revista: Clin Exp Immunol Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido

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