Pathogenesis of myositis in children

Thomas A. Griffin, Ann M. Reed

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

PURPOSE OF REVIEW: There is increasing evidence for involvement of innate immune mechanisms in the pathogenesis of idiopathic inflammatory myopathies. This review focuses on recent advances in understanding these mechanisms in juvenile dermatomyositis, the most common form of childhood inflammatory myopathy. RECENT FINDINGS: Type I interferon activity in juvenile dermatomyositis has been demonstrated by both global gene expression profiling and immunohistochemical analysis of affected tissues. Most recently, expression of interferon-inducible genes in peripheral blood cells has shown promise as a biomarker for disease activity. The possible pathogenic actions of type I interferons include induction and maintenance of major histocompatibility complex class I expression in affected myofibers, and promotion of local pro-inflammatory cytokine and chemokine production. The cellular source of type I interferons is not clearly defined, though plasmacytoid dendritic cells that constitute a significant component of the inflammatory cell infiltrate are obvious candidates. These cells likely contribute to pathogenesis not only via type I interferon production, but also by regulating other infiltrating inflammatory cells. SUMMARY: Type I interferons and plasmacytoid dendritic cells appear to make important contributions to the pathogenesis of juvenile dermatomyositis. Understanding the role of the innate immune system in childhood myositis may lead to novel treatment strategies.

Original languageEnglish (US)
Pages (from-to)487-491
Number of pages5
JournalCurrent Opinion in Rheumatology
Volume19
Issue number5
DOIs
StatePublished - Sep 2007

Fingerprint

Interferon Type I
Myositis
Dendritic Cells
Gene Expression Profiling
Cellular Structures
Major Histocompatibility Complex
Chemokines
Interferons
Immune System
Blood Cells
Biomarkers
Maintenance
Cytokines
Genes
Juvenile dermatomyositis

Keywords

  • Idiopathic inflammatory myopathies
  • Juvenile dermatomyositis
  • Plasmacytoid dendritic cells
  • Type I interferons

ASJC Scopus subject areas

  • Rheumatology
  • Immunology

Cite this

Pathogenesis of myositis in children. / Griffin, Thomas A.; Reed, Ann M.

In: Current Opinion in Rheumatology, Vol. 19, No. 5, 09.2007, p. 487-491.

Research output: Contribution to journalArticle

Griffin, Thomas A. ; Reed, Ann M. / Pathogenesis of myositis in children. In: Current Opinion in Rheumatology. 2007 ; Vol. 19, No. 5. pp. 487-491.
@article{65edca547ca94df9a160f1684b2c5c22,
title = "Pathogenesis of myositis in children",
abstract = "PURPOSE OF REVIEW: There is increasing evidence for involvement of innate immune mechanisms in the pathogenesis of idiopathic inflammatory myopathies. This review focuses on recent advances in understanding these mechanisms in juvenile dermatomyositis, the most common form of childhood inflammatory myopathy. RECENT FINDINGS: Type I interferon activity in juvenile dermatomyositis has been demonstrated by both global gene expression profiling and immunohistochemical analysis of affected tissues. Most recently, expression of interferon-inducible genes in peripheral blood cells has shown promise as a biomarker for disease activity. The possible pathogenic actions of type I interferons include induction and maintenance of major histocompatibility complex class I expression in affected myofibers, and promotion of local pro-inflammatory cytokine and chemokine production. The cellular source of type I interferons is not clearly defined, though plasmacytoid dendritic cells that constitute a significant component of the inflammatory cell infiltrate are obvious candidates. These cells likely contribute to pathogenesis not only via type I interferon production, but also by regulating other infiltrating inflammatory cells. SUMMARY: Type I interferons and plasmacytoid dendritic cells appear to make important contributions to the pathogenesis of juvenile dermatomyositis. Understanding the role of the innate immune system in childhood myositis may lead to novel treatment strategies.",
keywords = "Idiopathic inflammatory myopathies, Juvenile dermatomyositis, Plasmacytoid dendritic cells, Type I interferons",
author = "Griffin, {Thomas A.} and Reed, {Ann M.}",
year = "2007",
month = "9",
doi = "10.1097/BOR.0b013e32825a6a57",
language = "English (US)",
volume = "19",
pages = "487--491",
journal = "Current Opinion in Rheumatology",
issn = "1040-8711",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Pathogenesis of myositis in children

AU - Griffin, Thomas A.

AU - Reed, Ann M.

PY - 2007/9

Y1 - 2007/9

N2 - PURPOSE OF REVIEW: There is increasing evidence for involvement of innate immune mechanisms in the pathogenesis of idiopathic inflammatory myopathies. This review focuses on recent advances in understanding these mechanisms in juvenile dermatomyositis, the most common form of childhood inflammatory myopathy. RECENT FINDINGS: Type I interferon activity in juvenile dermatomyositis has been demonstrated by both global gene expression profiling and immunohistochemical analysis of affected tissues. Most recently, expression of interferon-inducible genes in peripheral blood cells has shown promise as a biomarker for disease activity. The possible pathogenic actions of type I interferons include induction and maintenance of major histocompatibility complex class I expression in affected myofibers, and promotion of local pro-inflammatory cytokine and chemokine production. The cellular source of type I interferons is not clearly defined, though plasmacytoid dendritic cells that constitute a significant component of the inflammatory cell infiltrate are obvious candidates. These cells likely contribute to pathogenesis not only via type I interferon production, but also by regulating other infiltrating inflammatory cells. SUMMARY: Type I interferons and plasmacytoid dendritic cells appear to make important contributions to the pathogenesis of juvenile dermatomyositis. Understanding the role of the innate immune system in childhood myositis may lead to novel treatment strategies.

AB - PURPOSE OF REVIEW: There is increasing evidence for involvement of innate immune mechanisms in the pathogenesis of idiopathic inflammatory myopathies. This review focuses on recent advances in understanding these mechanisms in juvenile dermatomyositis, the most common form of childhood inflammatory myopathy. RECENT FINDINGS: Type I interferon activity in juvenile dermatomyositis has been demonstrated by both global gene expression profiling and immunohistochemical analysis of affected tissues. Most recently, expression of interferon-inducible genes in peripheral blood cells has shown promise as a biomarker for disease activity. The possible pathogenic actions of type I interferons include induction and maintenance of major histocompatibility complex class I expression in affected myofibers, and promotion of local pro-inflammatory cytokine and chemokine production. The cellular source of type I interferons is not clearly defined, though plasmacytoid dendritic cells that constitute a significant component of the inflammatory cell infiltrate are obvious candidates. These cells likely contribute to pathogenesis not only via type I interferon production, but also by regulating other infiltrating inflammatory cells. SUMMARY: Type I interferons and plasmacytoid dendritic cells appear to make important contributions to the pathogenesis of juvenile dermatomyositis. Understanding the role of the innate immune system in childhood myositis may lead to novel treatment strategies.

KW - Idiopathic inflammatory myopathies

KW - Juvenile dermatomyositis

KW - Plasmacytoid dendritic cells

KW - Type I interferons

UR - http://www.scopus.com/inward/record.url?scp=34548335104&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34548335104&partnerID=8YFLogxK

U2 - 10.1097/BOR.0b013e32825a6a57

DO - 10.1097/BOR.0b013e32825a6a57

M3 - Article

C2 - 17762616

AN - SCOPUS:34548335104

VL - 19

SP - 487

EP - 491

JO - Current Opinion in Rheumatology

JF - Current Opinion in Rheumatology

SN - 1040-8711

IS - 5

ER -