TINAG – Dermatophytosis

Recent large-scale genome‑wide association studies (GWAS) have identified TINAG (HGNC:14599) as a susceptibility locus for dermatophytosis (MONDO_0004678). The analyses, conducted using the UK Biobank cohort, revealed genome‑wide significant association signals that implicate common variants in TINAG influencing the risk to develop dermatophytosis (PMID:35796184) and were independently supported in a follow‑up study (PMID:37592324).

Clinical validity for the association is rated as Strong. Both studies demonstrate robust statistical significance, with one report highlighting a top missense variant that increased the odds of dermatophytosis by up to 7.8 in homozygous carriers (PMID:35796184). Although the exact count of affected individuals or familial segregation details were not provided, the very large sample size and replication across independent analyses add compelling support.

The genetic evidence, while derived from population‐scale association data rather than single‐gene Mendelian cases, consolidates TINAG’s role in dermatophytosis susceptibility. No single variant formatted in standard HGVS nomenclature was directly detailed in these studies; rather, the association signal stems from a top SNP identified through GWAS. The overall inheritance pattern for this trait appears to be complex, reflecting multifactorial contributions as seen in common polygenic disorders.

In contrast, functional evidence remains limited. While TINAG performs various cellular roles, targeted experimental assays directly linking its function to the pathobiology of dermatophytosis have not been reported. The current evidence is entirely statistical in nature, creating an important gap for future mechanistic investigations.

Further studies, including cellular and animal models, are warranted to explore how TINAG influences host susceptibility to dermatophyte infections. Such work could shed light on potential immunological and skin barrier mechanisms that mediate this association and might reveal novel targets for prophylaxis or therapy.

In conclusion, the strong genetic evidence from independent GWAS strongly supports an association between TINAG and dermatophytosis. The integration of these findings with future functional data has the potential to enhance diagnostic decision‑making and guide personalized therapeutic strategies. Key take‑home sentence: TINAG represents a promising genetic marker for dermatophytosis risk, emphasizing its clinical utility in stratifying patients for subsequent management.

References

• Journal of the European Academy of Dermatology and Venereology • 2022 • Genome‑wide association study of dermatophytosis in the UK Biobank cohort PMID:35796184
• Mycoses • 2023 • Association of Kallikrein Related Peptidase 3 (KLK3) gene with dermatophytosis in the UK biobank cohort PMID:37592324

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