Value Proposition
· Promotes adenosine production to inhibit proinflammatory cytokine release
· Promotes regulatory T cells expansion
· Suppresses effector immune responses
· Amplifies a natural, local anti-inflammatory signal, which lowers risk of unintended side effects
· Targets specific inflammatory microenvironments to minimize systemic dysregulation
Unmet Need
· Many therapies for chronic diseases target inflammation to minimize further symptoms.
· Extracellular vesicles (EVs) are promising platforms for immunomodulatory therapies due to their intrinsic biological functions and versatility for molecular engineering.
· Additionally, current anti-inflammatory drugs are non-specific and affect broad pathways, which may have increased side effects.
· Thus, there is a need for a way to safely reprogram cells to produce targeted, anti-inflammatory signals at the protein level, providing a more natural and self-regulating method of therapy.
Technology Description
· Researchers at Johns Hopkins have developed EVs with genetically modified cells expressing CD39 and CD73 (EV-ADO) and the adhesion molecule PSGL-1 (EV-ADO-P).
· EV-ADO hydrolyzes pro-inflammatory ATP into adenosine, while EV-ADO-P facilitates EV targeting to inflamed environments.
· Functional assays demonstrated immunosuppressive effects of EV-ADO and EV-ADO-P in vitro, including reduced proinflammatory cytokine production, T cell proliferation, neutrophil oxidative burst, and platelet aggregation.
Stage of Development
· Validated in in vitro models utilizing macrophages, neutrophils, lymphocytes, and platelets.
Data Availability
· Data available upon request.
Publication
· N/A
