Michael S. Rogers

This study identifies IL-33 as a key mediator in endometriosis pain and lesion formation through neuroimmune communication involving CGRP and macrophages.

This study identifies M2 macrophages and IL1 signaling as key mediators of endometriosis risk and shows their pleiotropic role in comorbid traits.

This study investigates how adjuvant conditioning affects peritoneal macrophages and neutrophils, revealing a suppressive macrophage phenotype and enhanced neutrophil function.

This study identifies CMG2-actin interaction as essential for growth factor-induced chemotaxis in endothelial cells, showing that CMG2 binds F-actin to enable directional migration.

This study shows that adjuvant conditioning via alum induces immunosuppression through the NLRP3/IL-1 axis, promoting trained tolerance in allografts and human cells.

This study shows that blocking NGF-TrkA signaling reduces endometriosis-associated pain in mice, while blocking VEGF-VEGFR1 or BDNF-TrkB does not.

This study identifies CGRP/RAMP1 signaling as a driver of endometriosis pain and lesion growth, showing that blocking this pathway reduces pain and lesion size in mice.