CXCR2 signaling and host defense following coronavirus-induced encephalomyelitis.

Future Virology
Brett S MarroThomas E Lane

Abstract

Inoculation of the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the central nervous system (CNS) of susceptible strains of mice results in wide-spread replication within glial cells accompanied by infiltration of virus-specific T lymphocytes that control virus through cytokine secretion and cytolytic activity. Virus persists within white matter tracts of surviving mice resulting in demyelination that is amplified by inflammatory T cells and macrophages. In response to infection, numerous cytokines/chemokines are secreted by resident cells of the CNS and inflammatory leukocytes that participate in both host defense and disease. Among these are the ELR-positive chemokines that are able to signal through CXC chemokine receptors including CXCR2. Early following JHMV infection, ELR-positive chemokines contribute to host defense by attracting CXCR2-expressing cells including polymorphonuclear cells to the CNS that aid in host defense through increasing the permeability the blood-brain-barrier (BBB). During chronic disease, CXCR2 signaling on oligodendroglia protects these cells from apoptosis and restricts the severity of demyelination. This review covers aspects related to host defense and disease in response to JHMV ...Continue Reading

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Citations

Dec 24, 2014·Journal of Interferon & Cytokine Research : the Official Journal of the International Society for Interferon and Cytokine Research·Debjani GuhaVelpandi Ayyavoo
Jul 6, 2014·Frontiers in Cellular Neuroscience·Martin P Hosking, Thomas E Lane
Feb 9, 2021·Reviews in the Neurosciences·Dian Eurike Septyaningtrias, Rina Susilowati

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Methods Mentioned

BETA
transgenic

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis