ArticleMolecular biology reports2013
Polymorphisms and haplotypes in MyD88 are associated with the development of sarcoidosis: a candidate-gene association study.
Article in Molecular biology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Phenotypes and Endotypes in Sarcoidosis: Unraveling Prognosis and Disease Course.Biomedicines · 2025Review
- Pathogenetic Mechanisms Linking Sarcoidosis to Lymphoma.International journal of molecular sciences · 2025Review
- Innate and Adaptive Immunity in Noninfectious Granulomatous Lung Disease.Journal of immunology (Baltimore, Md. : 1950) · 2022Review
- The Immunogenetics of Granulomatous Diseases.Advances in experimental medicine and biology · 2022Article
- Adaptive Immunity in Pulmonary Sarcoidosis and Chronic Beryllium Disease.Frontiers in immunology · 2020Review
- Induction of Pulmonary Granuloma Formation by Propionibacterium acnes Is Regulated by MyD88 and Nox2.American journal of respiratory cell and molecular biology · 2017Article
- The -938C>A Polymorphism inDisease markers · 2016Article
- Immunogenetics of Disease-Causing Inflammation in Sarcoidosis.Clinical reviews in allergy & immunology · 2015Review
- Etiologies of Sarcoidosis.Clinical reviews in allergy & immunology · 2015Review
- Interleukin-12 family cytokines and sarcoidosis.Frontiers in pharmacology · 2014Review
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sarcoidosis is considered as a disorder of protracted immune response to an as yet unidentified causative agent that leads to granuloma formation. Material from M. tuberculosis and P. acne has been repeatedly detected in the sarcoidosis lesions, implying the involvement of the Toll-like receptor2 (TLR2) gene that responds to these intracellular pathogens. Since TLR2 association studies have produced controversial results, we sought to investigate whether the downstream signalling molecule MyD88 could be linked to disease susceptibility. We analyzed a total of 93 cases with sarcoidosis and of 89 controls for the most common MyD88 SNPs: -938C>A (rs4988453) and 1944C>G (rs4988457). There is evidence that the genotype distributions of both variants are associated with the development of sarcoidosis (p = 0.038 for -938C>A and p = 0.026 for 1944C>G). In particular, -938A and 1944G carriers were associated with risk of sarcoidosis [OR = 2.48 (1.23-5.02) and OR = 0.33 (0.14-0.76)], respectively, indicating dominance of the mutant alleles; however, the adjustment of the effect size for age and sex diminished the significance. The haplotype analysis showed association for the -938A/1944G haplotype (p < 0.001). Since genetic association studies have linked MyD88 to Hodgkin's lymphoma it is tempting to speculate that MyD88 may contribute to the granuloma formation that characterizes sarcoidosis.
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