Michael S. Rogers

Pro-endometriosis macrophage release of IL-33 is key for endometriosis pain and lesion formation

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

M2 Macrophages are Major Mediators of Germline Risk of Endometriosis and Explain Pleiotropy with Comorbid Traits

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

Adjuvant conditioning enhances neutrophil function while inducing a suppressive peritoneal macrophage phenotype

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

CMG2 interaction with actin is required for growth factor-induced chemotaxis in endothelial cells.

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.

Adjuvant conditioning shapes the adaptive immune response and promotes trained immunotolerance via NLRP3/IL-1

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

Nociceptor to macrophage communication through CGRP/RAMP1 signaling drives endometriosis-associated pain and lesion growth

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.