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Neonatal influenza-specific effector CTLs retain elevated CD31 levels at the site of infection and have decreased IFN-γ production
Journal article   Open access   Peer reviewed

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

Adam J Fike, Ogan K Kumova, Virginie J Tardif and Alison J Carey
Journal of leukocyte biology, v 105(3), pp 539-549
Mar 2019
DOI: https://doi.org/10.1002/JLB.4A0518-191R
PMID: 30536476
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1002/jlb.4a0518-191rView
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze),  Open
url
https://doi.org/10.1002/JLB.4A0518-191RView
Published, Version of Record (VoR) Open

Abstract

Animals Animals, Newborn Cell Proliferation Cell Survival CTLA-4 Antigen - metabolism Forkhead Transcription Factors - metabolism Interferon-gamma - biosynthesis Mice, Inbred C57BL Orthomyxoviridae Infections - immunology Orthomyxoviridae Infections - virology Platelet Endothelial Cell Adhesion Molecule-1 - metabolism Programmed Cell Death 1 Receptor - metabolism T-Lymphocytes, Cytotoxic - immunology Transcription Factors - metabolism Transcription, Genetic
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.

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6 citations in Web of Science
27 citations in Scopus

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UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being

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Collaboration types
Domestic collaboration
Web of Science research areas
Cell Biology
Hematology
Immunology
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