Abstract
BackgroundCD31, expressed by the majority of the neonatal T-cell pool, is involved in modulation of T-cell receptor signaling by increasing the threshold for T-cell activation. Therefore, CD31 could modulate neonatal tolerance and adaptive immune responses.MethodsLymphocytes were harvested from murine neonates at different ages, human late preterm and term cord blood, and adult peripheral blood. Human samples were activated over a 5-day period to simulate acute inflammation. Mice were infected with influenza; lungs and spleens were harvested at days 6 and 9 post infection and analyzed by flow cytometry.ResultsCD31-expressing neonatal murine CD4+ and CD8a+ T cells increase over the first week of life. Upon in vitro stimulation, human infants' CD4+ and CD8a+ T cells shed CD31 faster in comparison with adults. In the context of acute infection, mice infected at 3 days of age have an increased number of naive and activated CD31+ T lymphocytes at the site of infection at days 6 and 9 post infection, as compared with those infected at 7 days of age; however, the opposite is true in the periphery.ConclusionDifferences in trafficking of CD31+ cytotoxic T lymphocytes (CTLs) during acute influenza infection could modulate tolerance and contribute to a dampened adaptive immune response in neonates.