Neonatal influenza‐specific effector CTLs retain elevated CD31 levels at the site of infection and have decreased IFN‐γ production.

The underlying mechanisms that regulate neonatal immune suppression are poorly characterized. CD31 (PECAM1) is highly expressed on neonatal lymphocytes and is a known modulator of TCR signaling. To further characterize the role of CD31 in the neonatal CTL response, 3‐d and 7‐d‐old murine neonates were infected with influenza virus and compared to adults. The majority of the pulmonary viral‐specific CTLs in the 3‐d‐old murine neonate retain CD31 expression, whereas adult CTLs have decreased CD31 expression. In addition, CD31+ neonatal viral‐specific CTLs demonstrate decreased IFN‐γ production, decreased proliferative capacity, and increased likelihood of death. At the peak of infection, sorted neonatal effector CTLs continue to transcribe CD31, indicating a developmental regulation of expression. To explore potential mechanisms for this reduced function, we compared the expression of the transcription factors Eomesodermin (Eomes) and T‐bet; there was a significant increase in Eomes paired with a reduction in T‐bet in CD31+ neonatal effector CTLs in the lung. Furthermore, in vitro stimulated neonatal CTLs significantly reduce IFN‐γ production upon CD31 signaling. Altogether, these data indicate that neonatal CTLs may retain elevated levels of CD31 to maintain peripheral T cell suppression during the bridge to ex utero life. Murine neonatal influenza‐specific CD31+ effector CTLs have reduced IFN‐γ production, proliferation, and Tbet expression compared to adult counterparts. [ABSTRACT FROM AUTHOR]