tetano
Editor, Senior Moderator
J Leukoc Biol. 2018 Dec 11. doi: 10.1002/JLB.4A0518-191R. [Epub ahead of print]
[h=1]Neonatal influenza-specific effector CTLs retain elevated CD31 levels at the site of infection and have decreased IFN-γ production.[/h] Fike AJ[SUP]1,[/SUP][SUP]2[/SUP], Kumova OK[SUP]1[/SUP], Tardif VJ[SUP]3[/SUP], Carey AJ[SUP]1,[/SUP][SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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[SUP]+[/SUP] 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[SUP]+[/SUP] 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.
[h=4]KEYWORDS:[/h] CD31; CD8+ T cell; infections: respiratory viruses; neonate
PMID: 30536476 DOI: 10.1002/JLB.4A0518-191R
[h=1]Neonatal influenza-specific effector CTLs retain elevated CD31 levels at the site of infection and have decreased IFN-γ production.[/h] Fike AJ[SUP]1,[/SUP][SUP]2[/SUP], Kumova OK[SUP]1[/SUP], Tardif VJ[SUP]3[/SUP], Carey AJ[SUP]1,[/SUP][SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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[SUP]+[/SUP] 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[SUP]+[/SUP] 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.
[h=4]KEYWORDS:[/h] CD31; CD8+ T cell; infections: respiratory viruses; neonate
PMID: 30536476 DOI: 10.1002/JLB.4A0518-191R