Authors: Molin, S., Yeung, J., & Bissonnette, R
Different morphological and etiological subtypes of CHE appear to have overlapping and distinct features related to gene expression, proteomics, inflammatory biomarkers, and metagenomics, but data are limited and derived from small patient cohorts.
The available evidence points to the broad activation of immune pathways implicated in JAK-STAT signaling by receptors of the main cytokines including Th1, Th2, Th17, and Th22. Additional research is warranted to better understand the etiopathogenesis of CHE, which could ultimately uncover new treatment targets and facilitate personalized treatment selection.
