Abstract

Abstract CD31, expressed by the majority of the neonatal T cell pool, is involved in modulation of T-cell receptor (TCR) signalling by increasing the threshold for T cell activation. Therefore, CD31 could impact neonatal tolerance or immune responses during infection. Cells were harvested from murine neonates at various days post-birth, human late preterm and term cord blood and adult peripheral blood. The number of CD31 expressing CD4+ and CD8a+ T cells increase in the neonatal mouse over the first week of life, which is consistent with previous work demonstrating an increase in CD31 expression across human gestation. Human samples were activated in vitro over a five-day period to simulate acute inflammation similar to chorioamnionitis or early onset sepsis. The frequency of human CD31+ CD4+ and CD8a+ T cells decrease upon activation, with infants having a lower frequency of CD31+ cells compared to adults. In order to further evaluate the regulation of CD31 during acute infection, murine neonates at 3 and 7 days of age were infected with influenza. There was an increased number of naïve and activated CD31+ T lymphocytes at the site of infection at 6 and 9 days post-infection in the 3-day old neonates (p<0.05), as compared to 7-day old. However, the opposite is true in the periphery; mice infected at 7-days of age have an increased number of activated CD31+ T lymphocytes in the spleen at 9 days post-infection (p<0.05). Trafficking differences of CD31+T lymphocytes to the site of infection suggest a differential regulation in younger mice which could contribute to the dampened adaptive immune response in neonates. Further murine and human mechanistic studies which examine CD31+ cytotoxic T lymphocyte function at the site of infection are needed.

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