Rheumatoid factors.

T L Moore; R W Dorner

doi:10.1016/0009-9120(93)90032-2

Home/Archive/PubMed

PubMed · 8485860

Rheumatoid factors.

T L Moore·R W Dorner

View original source ↗Export metadata ↓

Abstract

Rheumatoid factors (RFs) have been studied for over 50 years and are probably the most written about of any antibody. Nevertheless, the etiology of these RFs and the precise role they play in the pathogenesis of rheumatoid arthritis (RA) and juvenile rheumatoid arthritis (JRA) remain a major interest. When RFs participate in the generation of inflammation in RA and JRA, they probably do so by forming immune complexes (IC) or are themselves able to bring about the inflammatory response. Their presence has been associated with more severe disease, vasculitis, and systemic symptoms. The present review summarises the literature over the last few years on new and interesting findings on RF. This review covers an update on RF assays, RF cross-reactivity, specificity studies, immune complex formation, RF lymphocyte studies, and RF binding.

Explore related subjects

Arthritis, Juvenile Arthritis, Rheumatoid Cross Reactions Humans Immunoglobulin G Immunoglobulin M Lymphocytes Rheumatoid Factor Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

T L Moore, R W Dorner. 1993. Rheumatoid factors.. https://doi.org/10.1016/0009-9120(93)90032-2

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

The role of ferroptosis in juvenile idiopathic arthritis: Causal inference and mediation by immune phenotypes.

This study employed a bidirectional 2-step, two-sample Mendelian randomization approach to investigate the causal relationships between ferroptosis-related genes and juvenile idiopathic arthritis (JIA) and to explore the mediating role of immune cells. Ferroptosis genes were identified from the deCODE database and matched with protein quantitative trait locus data as exposures to evaluate their causal effects on JIA, while immune cell traits were similarly assessed. For genes showing positive Mendelian randomization results, further analyses were conducted to determine whether immune cells mediated the effects on JIA, with mediation analysis performed only in the presence of causal associations. Data were sourced from the GWAS, FerrDb, and other public repositories. Nine ferroptosis-related genes were found to have causal links with JIA: HSPB1, DECR1, LIFR, and CTSB increased JIA risk, whereas PIEZO1, DPP4, BID, and others were protective. Forty immune cell traits were also causally associated with JIA. Mediation analysis revealed that several immune cells, including CD127- CD8+ T cells, partially mediated the genetic effects, with mediation proportions reaching up to 18.6%. Collectively, these results point to a ferroptosis-immune-JIA axis, suggesting that ferroptosis-related genes contribute to JIA pathogenesis through immune cell mediation and offering new mechanistic insights and potential therapeutic targets.

Arthritis, Juvenile↗

PubMed2026

Rare variant analysis of whole genome sequenced juvenile idiopathic arthritis multiplex pedigrees identifies rare variants in NOD2 and ACVR1.

Juvenile idiopathic arthritis is a complex rheumatic disease that is influenced by environmental and genetic factors. Linkage and genome-wide association studies have identified genes that contribute to the risk of developing juvenile idiopathic arthritis but are limited in their ability to identify disease-risk variants of large effect. Penetrant, heritable risk variants can be detected in high-risk families, but such cases are uncommon due to the low prevalence of juvenile idiopathic arthritis. This study utilizes whole-genome sequencing of 23 multiplex families, the largest such cohort to date, to discover variants and genes relevant to JIA pathogenesis. Pathogenic variants in NOD2 associated with Blau syndrome, an ultra-rare Mendelian inflammatory disorder, are the most recurrent variants in the cohort, consistent with previous reports that milder presentations of Blau syndrome are oftentimes misdiagnosed as juvenile idiopathic arthritis. For the first time, however, rare variants in ACVR1 and SMAD6, integral components of the Bone Morphogenic Protein pathway, are found to be associated with juvenile idiopathic arthritis. Identified ACVR1 variants map to critical protein domains. AlphaFold modeling predicts that the ACVR1 interaction with its inhibitor OGT is disrupted by these variants, indicating that the patient-mutated protein has a gain-of-function phenotype. Drosophila melanogaster expressing either a wild-type or patient-mutated version of ACVR1 exhibit embryonic lethality, with the mutant exhibiting 1.4-fold greater lethality than wild-type. The combination of family-based cohorts for gene discovery, AI-based computational tools, and animal model studies for tests of variant function underscores shared disease pathogenesis between JIA and monogenic disorders of immunity and connective tissue.

Arthritis, Juvenile↗

PubMed2006

Treatment of difficult cases of systemic-onset juvenile idiopathic arthritis with tacrolimus.

Since a proportion of systemic-onset juvenile idiopathic arthritis (SOJIA) patients continue to require long-term corticosteroid therapy for disease control, an effective and safe therapeutic strategy for controlling the activity of refractory SOJIA remains to be established. We report the efficacy of tacrolimus for the treatment of SOJIA in two patients with refractory SOJIA, one of them showing poor response to cyclosporine A. Tacrolimus might be the treatment of choice in selected patients with refractory systemic-onset juvenile idiopathic arthritis. Further studies to confirm the long-term efficacy and safety of tacrolimus in larger numbers of patients are, however, needed.

Arthritis, Juvenile↗