In vitro Autoreactivity against Skin and Synovial Cells in Patients with Juvenile Idiopathic and Rheumatoid Arthritis

Stechova, Katerina; Vavrincová, P; Chudoba, D; Frantlova, Miroslava; H, Reitzová; Sosna, A; Zimak, Jaroslav; Lednicky, Ladislav; Dickinson, Anne M.; Hromadníková, Ilona

doi:10.1159/000067306

Cited by 2 publications

(1 citation statement)

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“…(57) In a study of patients primarily with polyarticular JIA, peripheral blood cytotoxic T cells lysed autologous synovial cells and keratinocytes in vitro . (58) Mechanisms of loss of CD4 + and CD8 + T-cell tolerance to autoantigens could include molecular mimicry (that is, cross-reactive responses to self-peptides that resemble pathogen-derived peptides) and inflammation-induced epitope spreading.…”

Section: Pathogenesismentioning

confidence: 99%

Oligoarticular and polyarticular JIA: epidemiology and pathogenesis

et al. 2009

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Summary Juvenile idiopathic arthritis (JIA) refers to a group of chronic childhood arthropathies, currently classified into subtypes primarily on the basis of clinical features. Research has focused on the hypothesis that these subtypes arise through distinct etiologic pathways. In this Review, we discuss four subtypes of JIA: persistent oligoarticular, extended oligoarticular, rheumatoid-factor positive polyarticular and rheumatoid-factor-negative polyarticular. These subtypes differ in prevalence between ethnic groups and are associated with different HLA alleles. Non-HLA genetic risk factors have also been identified, some of which reveal further molecular differences between these subtypes, while others suggest mechanistic overlap. Investigations of immunophenotypes also provide insights into subtype differences: adaptive immunity appears to have a prominent role in both polyarticular and oligoarticular JIA, and the more-limited arthritis observed in persistent oligoarticular JIA as compared with extended oligoarticular JIA may reflect more-potent immunoregulatory T-cell activity in the former. Tumor necrosis factor seems to be a key mediator of both polyarticular and oligoarticular JIA, especially in the extended oligoarticular subtype, although elevated levels of other cytokines also are observed. Limited data on monocytes, dendritic cells, B cells, natural killer T cells, and neutrophils suggest that the contributions of these cells differ across subtypes of JIA. Within each subtype, however, common pathways appear to drive joint damage.

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Section: Pathogenesismentioning

confidence: 99%