HLA class II haplotype and autoantibody associations in children with juvenile dermatomyositis and juvenile dermatomyositis–scleroderma overlap

Wedderburn, Lucy R.; McHugh, Neil; Chinoy, Hector; Cooper, Robert G.; Salway, Fiona; Ollier, WE; McCann, Liza; Varsani, H; Dunphy, J. Englebert; North, J; Davidson, J. A.

doi:10.1093/rheumatology/kem265

Cited by 104 publications

(110 citation statements)

References 46 publications

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“…Since production of autoantibodies to muscle is pathognomonic for juvenile DM (29,30), we examined the differentiation state of the infiltrating B cells. In normal B cells, CD23, the low-affinity IgE receptor, indicates B cell maturation and differentiation to plasma cells (31).…”

mentioning

confidence: 99%

Extranodal lymphoid microstructures in inflamed muscle and disease severity of new‐onset juvenile dermatomyositis

Padilla¹,

Vallejo²,

Lacomis³

et al. 2009

Arthritis & Rheumatism

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Objective. Juvenile dermatomyositis (DM) is an autoimmune disease of childhood characterized by lesions in skin and muscle that are populated by plasmacytoid dendritic cells (PDCs) and lymphocyte infiltrates. We undertook this study to examine the cellular composition, organization, and molecular milieu of the cellular infiltrates in muscle in juvenile DM and to correlate the infiltrates with clinical disease manifestations.Methods. Since PDCs and lymphocyte foci express CCL19 and CCL21, we investigated for in situ formation of lymphoid microstructures that could be sites of extranodal immune activation.Results. Analyses of muscle biopsy samples from children with new-onset juvenile DM showed 3 categories of lesions: diffuse infiltrates, lymphocytic aggregates lacking follicle-like organization, and follicle-like structures. The last of these exhibited elements of classic lymphoid follicles, including networks of follicular dendritic cells and high endothelial venules. They also expressed high levels of CXCL13 and lymphotoxins known to support lymphoid organogenesis. There were also resident naive CD45RA؉ T cells and maternally derived B cells and PDCs. Patients with diffuse infiltrates or lymphocytic aggregates were responsive to standard therapy with steroids and methotrexate, but those with follicle-like structures tended to have severe disease that required additional agents such as intravenous Ig or rituximab.Conclusion. These data suggest that lymphoneogenesis is a component of the early disease process in juvenile DM. Ectopic lymphoid structures could indicate a severe course of disease; their early detection could be a tool for disease management.

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mentioning

confidence: 99%

Extranodal lymphoid microstructures in inflamed muscle and disease severity of new‐onset juvenile dermatomyositis

Padilla¹,

Vallejo²,

Lacomis³

et al. 2009

Arthritis & Rheumatism

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“…Relatively few cases of childhood SSc/myositis overlap have been reported 1,2,3,4,5,6,7 . In our case series, 4 patients diagnosed with juvenile overlap syndrome of myositis with SSc are described ( Table 1).…”

Section: Four Cases Of Anti-pm/scl Antibody-positive Juvenile Overlapmentioning

confidence: 99%

“…Overlap SSc/myositis has a relatively good prognosis 2,6 because of the typically mild myositis and good response to corticosteroids 9 . In our 3 patients with longer followup (an average of nearly 13 yrs), symptom control and eventually clinical remission were achieved (with normal muscle enzyme levels, normal muscle strength, and resolution of the JDM-associated rash), supporting a relatively favorable outcome.…”

Section: Four Cases Of Anti-pm/scl Antibody-positive Juvenile Overlapmentioning

confidence: 99%

Four Cases of Anti-PM/Scl Antibody-positive Juvenile Overlap Syndrome with Features of Myositis and Systemic Sclerosis

et al. 2016

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“…The tumour necrosis factor α variant, TNFα-308A, carries a higher risk of prolonged disease course, calcinosis and ulcerative skin disease, although there is controversy about whether this may be in part due to linkage disequilibrium with the HLA-B locus [Chinoy et al 2007]. The presence of the TNFα-308A allele in conjunction with an osteopontin promoter polymorphism (rs28357094G) has been found to be associated with high serum interferon-γ activity in the serum from untreated patients with JDM of European ancestry in a subset of patients who exhibit a more severe disease phenotype and are more likely to develop skin calcinosis.…”

Section: Geneticsmentioning

confidence: 99%

Juvenile dermatomyositis: new insights and new treatment strategies

Martin¹,

Li²,

Wedderburn³

2011

Therapeutic Advances in Musculoskeletal

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Juvenile dermatomyositis (JDM) is a rare but complex and potentially lifethreatening autoimmune disease of childhood, primarily affecting proximal muscles and skin. Although the cause of JDM remains unknown it is clear that genetic and environmental influences play a role in the aetiology. In contrast to adults with dermatomyositis, children with JDM are more likely to have complications that are thought to indicate a vasculopathic process, such as severe skin disease, with ulceration or calcinosis, gut vasculopathy or central nervous system disease. New treatments are much needed and are becoming available and being tested through international multicentre trials. This review will focus on recent insights into pathogenesis, the assessment of the disease in children and the modern approach to its treatment.

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HLA class II haplotype and autoantibody associations in children with juvenile dermatomyositis and juvenile dermatomyositis–scleroderma overlap

Cited by 104 publications

References 46 publications

Extranodal lymphoid microstructures in inflamed muscle and disease severity of new‐onset juvenile dermatomyositis

Extranodal lymphoid microstructures in inflamed muscle and disease severity of new‐onset juvenile dermatomyositis

Four Cases of Anti-PM/Scl Antibody-positive Juvenile Overlap Syndrome with Features of Myositis and Systemic Sclerosis

Juvenile dermatomyositis: new insights and new treatment strategies

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