AI Article Synopsis
- There is a potential genetic predisposition for individuals who are more susceptible to onychomycosis despite sharing the same environmental risk factors.
- Specific genetic mutations, particularly in the Dectin-1 immune receptors and certain human leukocyte antigen genotypes, are associated with higher rates of onychomycosis in affected families.
- Deficiencies in immune cells like CD4+CD25+ regulatory T cells can weaken the immune response, leading to chronic or recurrent fungal infections.
Article Abstract
Background: The variability in susceptibility to onychomycosis for individuals exposed to the same environmental risk factors raises the possibility that there may be individuals with a genetic predisposition to dermatophyte infection.
Objective: To determine whether there are genetic mutations or genotypes which contribute to onychomycosis.
Methods: The PubMed database was searched for examples of immune deficiencies resulting in dermatophyte infections.
Results: There are mutations in the innate immune receptors Dectin-1 and its adaptor protein CARD9 which result in familial mucocutaneous infections. There are also specific human leukocyte antigen genotypes that are more common in individuals and families with a high prevalence of onychomycosis. In addition, some patients have been reported with insufficient levels of CD4+CD25+ regulatory T cells. These deficits impair a full innate and adaptive immune response and may result in chronic or recurrent infections.
Conclusions: There are documented mutations and genotypes that contribute to familial and individual susceptibility to onychomycosis.
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| http://dx.doi.org/10.1159/000358586 | DOI Listing |
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