Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis
Moderate powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility.
A new model for an etiology of rheumatoid arthritis: smoking may trigger HLA-DR (shared epitope)-restricted immune reactions to autoantigens modified by citrullination.
An etiology involving a specific genotype, an environmental provocation, and the induction of specific autoimmunity are suggested, all restricted to a distinct subset of RA.
STAT4 and the risk of rheumatoid arthritis and systemic lupus erythematosus.
A haplotype of STAT4 is associated with increased risk for both rheumatoid arthritis and systemic lupus erythematosus, suggesting a shared pathway for these illnesses.
Epigenome-wide association data implicate DNA methylation as an intermediary of genetic risk in Rheumatoid Arthritis
DNA methylation is a potential mediator of genetic risk for rheumatoid arthritis and is corrected for cellular heterogeneity by estimating and adjusting for cell-type proportions in blood-derived DNA samples and used mediation analysis to filter out associations likely to be a consequence of disease.
Calculating measures of biological interaction
- T. Andersson, L. Alfredsson, H. Källberg, S. Zdravkovic, A. Ahlbom
- PhysicsEuropean Journal of Epidemiology
This article describes how a logistic regression model or a Cox regression model can be defined in order to produce the output that is needed for assessment of biological interaction and shows how common software can be programmed to deliver this output.
Genome-wide association study meta-analysis identifies seven new rheumatoid arthritis risk loci
Seven new rheumatoid arthritis risk alleles were identified at genome-wide significance (P < 5 × 10−8) in an analysis of all 41,282 samples, and an additional 11 SNPs replicated at P < 0.05, suggesting that most represent genuine rhearatoid arthritisrisk alleles.
Five amino acids in three HLA proteins explain most of the association between MHC and seropositive rheumatoid arthritis
Imputation of functional variation from large reference panels can help fine map association signals in the MHC, and three amino acid positions in HLA-DRβ1, which are all located in peptide-binding grooves, almost completely explain the M HC association to rheumatoid arthritis risk.
Replication of putative candidate-gene associations with rheumatoid arthritis in >4,000 samples from North America and Sweden: association of susceptibility with PTPN22, CTLA4, and PADI4.
Support is provided for PTPN22, CTLA4, and PADI4 as RA susceptibility genes and novel associations with clinically relevant subsets of RA are demonstrated.
Sleep disturbances, work stress and work hours: a cross-sectional study.
TRAF1-C5 as a risk locus for rheumatoid arthritis--a genomewide study.
A common genetic variant at the TRAF1-C5 locus on chromosome 9 is associated with an increased risk of anti-CCP-positive rheumatoid arthritis.