Unveiling the immunomodulatory shift: Epithelial-mesenchymal transition Alters immune mechanisms of amniotic cells

Epithelial-mesenchymal transition (EMT) changes cell phenotype by affecting immune properties of amniotic epithelial cells (AECs). The present study shows how the response to lipopolysaccharide of cells collected pre-(eAECs) and post-EMT (mAECs) induces changes in their transcriptomics profile. In fact, eAECs mainly upregulate genes involved in antigen-presenting response, whereas mAECs over-express soluble inflammatory mediator transcripts. Consistently, network analysis identifies CIITA and Nrf2 as main drivers of eAECs and mAECs immune response, respectively. As a consequence, the depletion of CIITA and Nrf2 impairs the ability of eAECs and mAECs to inhibit lymphocyte proliferation or macrophage-dependent IL-6 release, thus confirming their involvement in regulating immune response. Deciphering the mechanisms controlling the immune function of AECs pre-and post-EMT represents a step forward in understanding key physiological events wherein these cells are involved (pregnancy and labor). Moreover, controlling the immunomodulatory properties of eAECs and mAECs may be

Automated summary

This study reveals the impact of epithelial-mesenchymal transition (EMT) on the immune properties of amniotic epithelial cells (AECs). The response to lipopolysaccharide differs between pre-EMT (eAECs) and post-EMT (mAECs), with eAECs upregulating genes involved in antigen-presenting response and mAECs over-expressing soluble inflammatory mediator transcripts. Network analysis identifies CIITA and Nrf2 as the main drivers of eAECs and mAECs immune response, respectively.