Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Mapping of a candidate region for susceptibility to inclusion body myositis in the human major histocompatibility complex.

Immunogenetics - 1 Jun 1999

Kok C C, Croager E J, Witt C S, Kiers L, Mastaglia F L, Abraham L J, Garlepp M J

Abstract excerpt

Inclusion body myositis (IBM) is a form of idiopathic inflammatory myopathy of unknown aetiology. A strong association with HLA class II (HLA-DR3) suggested a role for genes in the human major histocompatibility complex (MHC) in the predisposition to this disease. In this study, we have taken advantage of the ancestral haplotype (AH) concept and historical recombinations to map for a possible susceptibility...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Chromosome Mapping
Share to HSP70 Heat-Shock Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Major Histocompatibility Complex

Share to Microsatellite Repeats

Share to Myositis, Inclusion Body

Share to Polymorphism, Restriction Fragment Length

Share to Polymorphism, Single-Stranded Conformational

Share to Tumor Necrosis Factor-alpha

Source

Identifiers

PMID: 10380695
DOI: 10.1007/s002510050528

Genes

TNF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mapping of a candidate region for susceptibility to inclusion body myositis in the human major histocompatibility complex.PMID 10380695Read ↗

Immunogenetics of Idiopathic Inflammatory Myopathies: The Role of HLA Genes Within and Beyond the Ancestral Haplotype.Semantic proximity Read ↗

Immunogenetic risk and protective factors for the idiopathic inflammatory myopathies: distinct HLA-A, -B, -Cw, -DRB1 and -DQA1 allelic profiles and motifs define clinicopathologic groups in caucasians.Semantic proximity Read ↗

Immune-Array Analysis in Sporadic Inclusion Body Myositis Reveals HLA-DRB1 Amino Acid Heterogeneity Across the Myositis Spectrum.Semantic proximity Read ↗

Recombination mapping of the susceptibility region for sporadic inclusion body myositis within the major histocompatibility complex.Semantic proximity Read ↗

An update on the immunogenetics of idiopathic inflammatory myopathies: major histocompatibility complex and beyond.Semantic proximity Read ↗

High-resolution HLA genotyping in inclusion body myositis refines 8.1 ancestral haplotype association to DRB1*03:01:01 and highlights pathogenic role of arginine-74 of DRβ1 chain.Semantic proximity Read ↗

Two major histocompatibility complex haplotypes influence susceptibility to sporadic inclusion body myositis: critical evaluation of an association with HLA-DR3.Semantic proximity Read ↗

Immunogenetic risk and protective factors for the idiopathic inflammatory myopathies: distinct HLA-A, -B, -Cw, -DRB1, and -DQA1 allelic profiles distinguish European American patients with different myositis autoantibodies.Semantic proximity Read ↗

New developments in genetics of myositis.Semantic proximity Read ↗

Sporadic inclusion body myositis: variability in prevalence and phenotype and influence of the MHC.Semantic proximity Read ↗

Sporadic inclusion body myositis in Japanese is associated with the MHC ancestral haplotype 52.1.Semantic proximity Read ↗

Genome-wide association study identifies HLA 8.1 ancestral haplotype alleles as major genetic risk factors for myositis phenotypes.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.