ArticleArthritis and rheumatism2008
Immunoglobulin gene polymorphisms are susceptibility factors in clinical and autoantibody subgroups of the idiopathic inflammatory myopathies.
Article in Arthritis and rheumatism, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Association betweenFrontiers in immunology · 2026Article
- Immunoglobulin GM (γ marker) allotypes and their role in immune response and disease susceptibility.Journal of immunology (Baltimore, Md. : 1950) · 2025Review
- A possible role for immunogenetic factors in myositis developing after vaccination in the pre-covid-19 era.Frontiers in immunology · 2025Article
- Genetic Influences in Cancer-Associated Myositis.Arthritis & rheumatology (Hoboken, N.J.) · 2023Review
- The phenotype of myositis patients with anti-Ku autoantibodies.Seminars in arthritis and rheumatism · 2021Article
- NanoString technology distinguishes anti-TIF-1γBrain pathology (Zurich, Switzerland) · 2021Article
- Dermatomyositis autoantibodies: how can we maximize utility?Annals of translational medicine · 2021Review
- FcγR Binding and ADCC Activity of Human IgG Allotypes.Frontiers in immunology · 2020Article
- The Ligands for Human IgG and Their Effector Functions.Antibodies (Basel, Switzerland) · 2019Review
- Race, Income, and Disease Outcomes in Juvenile Dermatomyositis.The Journal of pediatrics · 2017Article
- Idiopathic Inflammatory Myopathies: an Update on Classification and Treatment with Special Focus on Juvenile Forms.Clinical reviews in allergy & immunology · 2017Review
- Brief Report: Association of Myositis Autoantibodies, Clinical Features, and Environmental Exposures at Illness Onset With Disease Course in Juvenile Myositis.Arthritis & rheumatology (Hoboken, N.J.) · 2016Article
- Positive association of genetic variations in the phospholipase C-like 1 gene with dermatomyositis in Chinese Han.Immunologic research · 2016Article
- Clinical course and outcomes of Iranian children with juvenile dermatomyositis and polymyositis.Clinical rheumatology · 2014Article
- Implications in the difference of anti-Mi-2 and -p155/140 autoantibody prevalence in two dermatomyositis cohorts from Mexico City and Guadalajara.Arthritis research & therapy · 2013Article
- The forgotten tale of immunoglobulin allotypes in cancer risk and treatment.Experimental hematology & oncology · 2013Article
- Mass spectrometric determination of IgG subclass-specific glycosylation profiles in siblings discordant for myositis syndromes.Journal of proteome research · 2011Article
- Autoimmune myopathies: autoantibodies, phenotypes and pathogenesis.Nature reviews. Neurology · 2011Review
- Recent advances in the immunogenetics of idiopathic inflammatory myopathy.Arthritis research & therapy · 2011Review
- Immunoglobulin locus associates with serum IgG levels and albuminuria.Journal of the American Society of Nephrology : JASN · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveTo investigate possible associations of GM and KM markers with adult and juvenile forms of the idiopathic inflammatory myopathies (IIMs) in Caucasian and African American patients.
methodsWe performed serologic analyses of polymorphic determinants associated with immunoglobulin gamma heavy chains (GM) and kappa light chains (KM) in large populations of Caucasian patients (n= 514 [297 adults and 217 children]) and African American patients (n=123 [73 adults and 50 children]) with IIM representing the major clinical and autoantibody groups.
resultsFor Caucasian patients with dermatomyositis (DM), the Gm 3 23 5,13 phenotype was a risk factor in both adults (odds ratio [OR] 2.2, corrected P [Pcorr]=0.020) and children (OR 2.2, Pcorr=0.0013). Of interest, the GM 13 allotype was a risk factor for juvenile DM in both Caucasian subjects (OR 3.9, Pcorr<0.0001) and African American subjects (OR 4.8, Pcorr=0.033). However, the Gm 1,3,17 5,13,21 phenotype was a risk factor for juvenile DM in Caucasian subjects but not African American subjects. Among the IIM autoantibody groups, Gm 3 23 5,13 was a risk factor in Caucasian adults with anti-Jo-1 autoantibodies (OR 3.4, Pcorr=0.0031), while the GM 3 allotype was protective in adults with anti-threonyl-transfer RNA synthetase or anti-U RNP autoantibodies (OR 0.1, Pcorr=0.047 and OR 0.2, Pcorr=0.034, respectively). In contrast, GM 6 was a risk factor in African American adults with anti-signal recognition particle autoantibodies (OR 7.5, Pcorr=0.041).
conclusionThese data suggest that polymorphic alleles of GM and KM loci are differentially associated with IIM subgroups defined by age, ethnicity, clinical features, and autoantibody status, and expand the list of immune response genes that are possibly important in the pathogenesis of myositis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.