About: PD-1 Dynamically Regulates Inflammation and Development of Brain-Resident Memory CD8 T Cells During Persistent Viral Encephalitis

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About: PD-1 Dynamically Regulates Inflammation and Development of Brain-Resident Memory CD8 T Cells During Persistent Viral Encephalitis Goto Sponge NotDistinct Permalink

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Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	PD-1 Dynamically Regulates Inflammation and Development of Brain-Resident Memory CD8 T Cells During Persistent Viral Encephalitis
Creator	Shwetank, Toprak, Mesut Frost, Elizabeth Campbell, Iain Evavold, Brian Lokensgard, James Lukacher, Aron Mockus, Taryn Ren, Heather Lauver, Matthew Cosby, Jennifer Feng, Carl Netherby-Winslow, Colleen
source	Medline; PMC
abstract	Programmed cell death-1 (PD-1) receptor signaling dampens the functionality of T cells faced with repetitive antigenic stimulation from chronic infections or tumors. Using intracerebral (i.c.) inoculation with mouse polyomavirus (MuPyV), we have shown that CD8 T cells establish a PD-1(hi), tissue-resident memory population in the brains (bT(RM)) of mice with a low-level persistent infection. In MuPyV encephalitis, PD-L1 was expressed on infiltrating myeloid cells, microglia and astrocytes, but not on oligodendrocytes. Engagement of PD-1 on anti-MuPyV CD8 T cells limited their effector activity. NanoString gene expression analysis showed that neuroinflammation was higher in PD-L1(−/−) than wild type mice at day 8 post-infection, the peak of the MuPyV-specific CD8 response. During the persistent phase of infection, however, the absence of PD-1 signaling was found to be associated with a lower inflammatory response than in wild type mice. Genetic disruption and intracerebroventricular blockade of PD-1 signaling resulted in an increase in number of MuPyV-specific CD8 bT(RM) and the fraction of these cells expressing CD103, the αE integrin commonly used to define tissue-resident T cells. However, PD-L1(−/−) mice persistently infected with MuPyV showed impaired virus control upon i.c. re-infection with MuPyV. Collectively, these data reveal a temporal duality in PD-1-mediated regulation of MuPyV-associated neuroinflammation. PD-1 signaling limited the severity of neuroinflammation during acute infection but sustained a level of inflammation during persistent infection for maintaining control of virus re-infection.
has issue date	2019-04-17(xsd:dateTime)
bibo:doi	10.3389/fimmu.2019.00783
bibo:pmid	31105690
has license	cc-by
sha1sum (hex)	20ae5549ea5761744ffac3015a31a03816699a49
schema:url	https://doi.org/10.3389/fimmu.2019.00783
resource representing a document's title	PD-1 Dynamically Regulates Inflammation and Development of Brain-Resident Memory CD8 T Cells During Persistent Viral Encephalitis
has PubMed Central identifier	PMC6499176
has PubMed identifier	31105690
schema:publication	Front Immunol
resource representing a document's body	covid:20ae5549ea5761744ffac3015a31a03816699a49#body_text
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