We are analyzing https://link.springer.com/article/10.1007/s12016-012-8346-7.

Title:
Genetics of Rheumatoid Arthritis — A Comprehensive Review | Clinical Reviews in Allergy & Immunology
Description:
The “Bermuda triangle” of genetics, environment and autoimmunity is involved in the pathogenesis of rheumatoid arthritis (RA). Various aspects of genetic contribution to the etiology, pathogenesis and outcome of RA are discussed in this review. The heritability of RA has been estimated to be about 60 %, while the contribution of HLA to heritability has been estimated to be 11–37 %. Apart from known shared epitope (SE) alleles, such as HLA-DRB1*01 and DRB1*04, other HLA alleles, such as HLA-DRB1*13 and DRB1*15 have been linked to RA susceptibility. A novel SE classification divides SE alleles into S1, S2, S3P and S3D groups, where primarily S2 and S3P groups have been associated with predisposition to seropositive RA. The most relevant non-HLA gene single nucleotide polymorphisms (SNPs) associated with RA include PTPN22, IL23R, TRAF1, CTLA4, IRF5, STAT4, CCR6, PADI4. Large genome-wide association studies (GWAS) have identified more than 30 loci involved in RA pathogenesis. HLA and some non-HLA genes may differentiate between anti-citrullinated protein antibody (ACPA) seropositive and seronegative RA. Genetic susceptibility has also been associated with environmental factors, primarily smoking. Some GWAS studies carried out in rodent models of arthritis have confirmed the role of human genes. For example, in the collagen-induced (CIA) and proteoglycan-induced arthritis (PgIA) models, two important loci — Pgia26/Cia5 and Pgia2/Cia2/Cia3, corresponding the human PTPN22/CD2 and TRAF1/C5 loci, respectively — have been identified. Finally, pharmacogenomics identified SNPs or multiple genetic signatures that may be associated with responses to traditional disease-modifying drugs and biologics.
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Keywords {🔍}

arthritis, article, rheumatoid, google, scholar, pubmed, cas, rheum, genetic, anticitrullinated, protein, epitope, rheumatol, shared, van, risk, alleles, gene, genetics, szekanecz, hladrb, association, rev, diseases, patients, susceptibility, nat, clin, contribution, loci, factors, huizinga, citrullinated, antibodies, data, glant, polymorphisms, genomewide, smoking, access, study, genet, ann, associations, medical, privacy, cookies, content, european, research,

Topics {✒️}

anti-citrullinated protein antibody-positive anti-citrullinated protein/peptide autoantibodies quantitative trait loci anti-citrullinated protein antibody genome-wide association study single-nucleotide polymorphism month download article/chapter serum anti-ccp antibody central-eastern european cohort anti-cyclic citrullinated peptide anti-citrullinated protein antibodies anti-citrullinated peptide antibodies anti-tumour necrosis factors de vries-bouwstra jk traditional disease-modifying drugs il-1rn gene polymorphisms murine autoimmune arthritis gene–environment interaction influences van gaalen fa animal models gwas studies carried article clinical reviews hla-drb1 alleles supports hla-shared epitope alleles glant & katalin mikecz cyclic citrullinated peptide hla-dr genotypes hla-drb1 shared epitope full article pdf immune-mediated inflammatory diseases quantitative genetic contribution genome-wide searching shared epitope allele protein plasma levels cyclic citrullinated peptides privacy choices/manage cookies genetic risk factor de vries rr gene expression profiles gene expression profiling methotrexate-related elevation lifestyle-related factors chemokine receptor blockade hla-dr4 expression methylenetetrahydrofolate reductase gene medical research council rheumatoid factor levels hla-dr hla-shared epitope acpa-negative ra

Questions {❓}

Bax M, van Heemst J, Huizinga TW, Toes RE (2011) Genetics of rheumatoid arthritis: what have we learned?
Daha NA, Toes RE (2011) Rheumatoid arthritis: Are ACPA-positive and ACPA-negative RA the same disease?
Genetic markers as therapeutic target in rheumatoid arthritis: A game changer in clinical therapy?
Szekanecz Z, Soos L, Szabo Z, Fekete A, Kapitany A, Vegvari A et al (2008) Anti-citrullinated protein antibodies in rheumatoid arthritis: as good as it gets?

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         headline:Genetics of Rheumatoid Arthritis — A Comprehensive Review
         description:The “Bermuda triangle” of genetics, environment and autoimmunity is involved in the pathogenesis of rheumatoid arthritis (RA). Various aspects of genetic contribution to the etiology, pathogenesis and outcome of RA are discussed in this review. The heritability of RA has been estimated to be about 60 %, while the contribution of HLA to heritability has been estimated to be 11–37 %. Apart from known shared epitope (SE) alleles, such as HLA-DRB1*01 and DRB1*04, other HLA alleles, such as HLA-DRB1*13 and DRB1*15 have been linked to RA susceptibility. A novel SE classification divides SE alleles into S1, S2, S3P and S3D groups, where primarily S2 and S3P groups have been associated with predisposition to seropositive RA. The most relevant non-HLA gene single nucleotide polymorphisms (SNPs) associated with RA include PTPN22, IL23R, TRAF1, CTLA4, IRF5, STAT4, CCR6, PADI4. Large genome-wide association studies (GWAS) have identified more than 30 loci involved in RA pathogenesis. HLA and some non-HLA genes may differentiate between anti-citrullinated protein antibody (ACPA) seropositive and seronegative RA. Genetic susceptibility has also been associated with environmental factors, primarily smoking. Some GWAS studies carried out in rodent models of arthritis have confirmed the role of human genes. For example, in the collagen-induced (CIA) and proteoglycan-induced arthritis (PgIA) models, two important loci — Pgia26/Cia5 and Pgia2/Cia2/Cia3, corresponding the human PTPN22/CD2 and TRAF1/C5 loci, respectively — have been identified. Finally, pharmacogenomics identified SNPs or multiple genetic signatures that may be associated with responses to traditional disease-modifying drugs and biologics.
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