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Evidence for the role of IL26 in multiple sclerosis (MS) is emerging from two independent multi‐patient studies. In one study a broad panel of genes, including IL26, was interrogated in MS cohorts comprising over 800 patients (PMID:18332247) and in a separate analysis IL26 was among several candidates identified by whole‐exome sequencing in MS families with vertical transmission (PMID:35008743). Although the strongest susceptibility signals were confined to neighboring genes such as IFNG, the inclusion of IL26 in these analyses suggests that it may participate in the regulatory network contributing to MS risk. Notably, no IL26‐specific variants or segregation data have been reported, limiting the strength of the genetic evidence.
A functional study in the dromedary camel further demonstrated the existence of multiple transcript variants of IL26 produced by alternative splicing (PMID:26190308). This experiment provides preliminary insight into the molecular regulation of IL26; however, its direct relevance to MS pathogenesis remains to be established. Given the current observations, the available evidence supports only a limited association between IL26 and MS. Additional focused genetic and functional studies in human cohorts are warranted to clarify the clinical utility of IL26 as a diagnostic marker or therapeutic target.
Gene–Disease AssociationLimitedIL26 was noted in multi‐gene panels from MS cohorts (PMID:35008743), but no IL26‐specific causal variants or segregation data have been reported. Genetic EvidenceLimitedIL26 appears as part of candidate gene lists in genomic screens with MS patients, yet direct variant-level evidence supporting its role is lacking (PMID:35008743). Functional EvidenceLimitedA functional study in a non-human model revealed alternative splicing events in IL26 (PMID:26190308), though the impact on MS pathogenesis remains unclear. |