During antibody responses, B cells undergo a series of migratory events that guide them to the appropriate micro environments for activation and differentiation. EBI2 plays an important role in coordinating rapid versus long term humoral responses as proliferating B cells begin to follow one of two alternate fates: differentiation into plasma cells or germinal center (GC) B cells. Several studies linked EBI2 expression to human neoplastic diseases, such as acute myeloid leukemia, chronic lymphocytic leukemia and diffuse large B cell lymphoma. In collaboration with Robert Rickert, the EBI2 research program has investigated mechanisms by which perturbations in EBI2 effect immune-mediated inflammatory disease.
PCT WO 2015048570 “EBI-2 modulators” Pinkerton, A. B.; Ardecky, R.; Serguienko, E. A.; Gonzalez-Lopez, M.; Ganji, S. R.; Zou, J.
PCT WO 2015048567 “Spirocyclic EBI-2 modulators” Pinkerton, A. B.; Ardecky, R.; Serguienko, E. A.; Gonzalez-Lopez, M.; Ganji, S. R.; Zou, J.
Functional Antagonists of EBI2/GPR183 as Chemical Probes for Inflammation, Collaboration with Robert Rickert and the Conrad Prebys Center for Chemical Genomics