ArticleFrontiers in immunology2026
Long noncoding RNA associations with an IFI27-MCEMP1 transcript pattern in Kawasaki disease.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Kawasaki disease (KD) is an acute pediatric vasculitis with risk of coronary artery injury. A two-transcript IFI27-MCEMP1 score has distinguished KD from other febrile illnesses, but its relationship to long noncoding RNAs (lncRNAs) is incompletely defined. We evaluated whether peripheral blood mononuclear cell (PBMC) lncRNA expression differed between KD and febrile controls and was associated with the IFI27-MCEMP1 transcript pattern. Children younger than 8 years were prospectively enrolled at the Children's Hospital of Fudan University during 2024-2025. The newly enrolled cohort included 55 children with KD and 48 febrile controls; integration with two same-site cohorts yielded 188 children with KD and 175 febrile controls. Bulk-PBMC expression of IFI27, MCEMP1, CHROMR, MALAT1, and NEAT1 was measured by reverse transcription quantitative PCR and normalized to GAPDH. The prespecified score distinguished KD from febrile controls with areas under the receiver operating characteristic curve of 0.88 (95% CI, 0.80-0.95) in the newly enrolled cohort and 0.89 (95% CI, 0.86-0.93) in the integrated cohort. In unadjusted integrated analyses, CHROMR and MALAT1 expression was lower in KD, whereas NEAT1 did not differ significantly. CHROMR ΔCt correlated with IFI27 ΔCt (r=0.55; Holm-adjusted P<.001). After adjustment for fever duration and a CBC-derived monocyte fraction, lower CHROMR and IFI27 and higher MCEMP1 expression remained significant, whereas the MALAT1 difference was attenuated. Exact fever-day matching yielded concordant CHROMR, IFI27, and MCEMP1 group differences, but the adjusted CHROMR-IFI27 correlation was not significant in the restricted matched population. Thus, KD was associated with a bulk-PBMC transcript pattern involving CHROMR, IFI27, and MCEMP1; the MALAT1 finding was less robust. These associations motivate hypotheses about interferon-associated and myeloid-associated biology but do not establish pathway activity or causality. Multicenter studies with standardized sampling, cell-resolved profiling, and independent CHROMR assay confirmation are required.
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