RESUMEN
In transplantation, immunosuppression has been directed at controlling acute responses, but treatment of chronic rejection has been ineffective. It is possible that factors that have previously been unaccounted for, such as exposure to inhaled pollution, ultraviolet light, or loss of the normal equilibrium between the gut immune system and the outside environment may be responsible for shifting immune responses to an effector/inflammatory phenotype, which leads to loss of self-tolerance and graft acceptance, and a shift towards autoimmunity and chronic rejection. Cells of the immune system are in a constant balance of effector response, regulation, and quiescence. Endogenous and exogenous signals can shift this balance through the aryl hydrocarbon receptor, which serves as a thermostat to modulate the response one way or the other, both at mucosal surfaces of interface organs to the outside environment, and in the internal milieu. Better understanding of this balance will identify a target for maintenance of self-tolerance and continued graft acceptance in patients who have achieved a "steady state" after transplantation.
Asunto(s)
Exposición a Riesgos Ambientales/efectos adversos , Rechazo de Injerto/etiología , Tolerancia Inmunológica/inmunología , Trasplante de Órganos/efectos adversos , Animales , HumanosRESUMEN
Two patients presented in profound respiratory distress unresponsive to maximal support and were placed on venovenous ECMO. Subsequently, both were found to have a patent foramen ovale and high pulmonary artery pressures, resulting in a right to left shunt. Both patients had a better than expected response to ECMO, likely related to their shunts allowing oxygenated blood to bypass the high pulmonary artery pressures and go directly to the left heart. Both patients were successfully weaned from ECMO and discharged to home in good condition.