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Infant’s immune system cannot control infection or respond to vaccination as efficiently as older individuals, a phenomenon that has been attributed to immunological immaturity. Recently, we challenged this notion and proposed the presence of actively immunosuppressive and physiologically enriched CD71 +  erythroid cells in neonates. Here we utilized  Bordetella pertussis , a common neonatal respiratory tract pathogen, as a proof of concept to investigate the role of these cells in adaptive immunity. We observed that CD71 +  cells have distinctive immunosuppressive properties and prevent recruitment of immune cells to the mucosal site of infection. CD71 +  cells ablation unleashed induction of  B. pertussis -specific protective cytokines (IL-17 and IFN-γ) in the lungs and spleen upon re-infection or vaccination. We also found that CD71 +  cells suppress systemic and mucosal  B. pertussis -specific antibody responses. Enhanced antigen-specific adaptive immunity following CD71 +  cells depletion increased resistance of mice to  B. pertussis  infection. Furthermore, we found that human cord blood CD71 +  cells also suppress T and B cell functions  in vitro . Collectively, these data provide important insight into the role of CD71 +  erythroid cells in adaptive immunity. We anticipate our results will spark renewed investigation in modulating the function of these cells to enhance host defense to infections in newborns.

CD71+ erythroid suppressor cells impair adaptive immunity against Bordetella pertussis