Transcriptome profile within the mouse central nervous system and activation of myelin-reactive T cells following murine coronavirus infection

Gruslin, Edith; Moisan, Steve; St‐Pierre, Yves; Desforges, Marc; Talbot, Pierre J.

doi:10.1016/j.jneuroim.2005.01.007

Cited by 11 publications

(11 citation statements)

References 52 publications

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“…Cytotoxic T lymphocytes attracted to the CNS during a murine coronavirus (MHV) infection need the help of the CD4 + population to be effective in clearing the virus from the CNS [46]. Moreover, we have recently demonstrated that MBP-reactive T cells were activated following MHV-A59 infection of the CNS [47]. Therefore, such CD4+ cells may also be essential to clear neuroinvasive HCoV [12] from the CNS and could react against myelin epitopes being exposed in significant concentrations after damage resulting from inflammation brought about by virus-mediated activation of glial cells, cytokines and nitric oxide [48].…”

Section: Discussionmentioning

confidence: 99%

Long-term human coronavirus-myelin cross-reactive T-cell clones derived from multiple sclerosis patients

Boucher

Desforges

Duquette

et al. 2007

Clinical Immunology

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Autoimmune reactions associated with MS involve genetic and environmental factors. Because murine coronaviruses induce an MS-like disease, the human coronaviruses (HCoV) are attractive candidates as environmental factors involved in a demyelinating pathology. We previously reported the isolation of HCoV-229E/myelin basic protein (MBP) cross-reactive T-cell lines (TCL) in MS patients. To investigate antigenic cross-reactivity at the molecular level, 155 long-term T-cell clones (TCC) were derived from 32 MS patients by in vitro selection with MBP, proteolipid protein (PLP) or HCoV (strains 229E and OC43). Overall, 114 TCC were virus-specific, 31 were specific for myelin Ag and 10 other were HCoV/myelin cross-reactive. Twenty-eight virus-specific TCC and 7 myelin-specific TCC were obtained from six healthy donors. RACE RT-PCR amplification of the Vbeta chains of five of ten the cross-reactive TCC confirmed clonality and sequencing identified the CDR3 region associated with cross-reactivity. Our findings have promising implications in the investigation of the role of molecular mimicry between coronaviruses and myelin in MS as a mechanism related to disease initiation or relapses.

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Section: Discussionmentioning

confidence: 99%

Long-term human coronavirus-myelin cross-reactive T-cell clones derived from multiple sclerosis patients

Boucher

Desforges

Duquette

et al. 2007

Clinical Immunology

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“…SR T cell accumulation within the CNS of infected mice was shown to peak in mice persistently infected with JHMV; yet, these cells were not retained arguing for minimal pathologic function. In addition, a recent report has suggested that infection with mouse hepatitis virus strain A59 promotes activation of autoreactive T cells specific to myelin basic protein, although the contributions of these cells to demyelination remain to be fully defined (25).…”

Section: Jhmv-induced Demyelinationmentioning

confidence: 99%

Chemokine CXCL10 and Coronavirus-Induced Neurologic Disease

2019

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Chemokines (chemotactic cytokines) are involved in a wide variety of biological processes. Following microbial infection, there is often robust chemokine signaling elicited from infected cells, which contributes to both innate and adaptive immune responses that control growth of the invading pathogen. Infection of the central nervous system (CNS) by the neuroadapted John Howard Mueller (JHM) strain of mouse hepatitis virus (JHMV) provides an excellent example of how chemokines aid in host defense as well as contribute to disease. Intracranial inoculation of the CNS of susceptible mice with JHMV results in an acute encephalomyelitis characterized by widespread dissemination of virus throughout the parenchyma. Virus-specific T cells are recruited to the CNS, and control viral replication through release of antiviral cytokines and cytolytic activity. Sterile immunity is not acquired, and virus will persist primarily in white matter tracts leading to chronic neuroinflammation and demyelination. Chemokines are expressed and contribute to defense as well as chronic disease by attracting targeted populations of leukocytes to the CNS. The T cell chemoattractant chemokine CXCL10 (interferon-inducible protein 10 kDa, IP-10) is prominently expressed in both stages of disease, and serves to attract activated T and B lymphocytes expressing CXC chemokine receptor 3 (CXCR3), the receptor for CXCL10. Functional studies that have blocked expression of either CXCL10 or CXCR3 illuminate the important role of this signaling pathway in host defense and neurodegeneration in a model of viral-induced neurologic disease.

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“…Whether a similar response occurs in MHV-infected mice and what the contributions are to demyelination are unknown at this time. A recent report has suggested that infection with MHV strain A59 promotes the activation of autoreactive T cells specific to myelin basic protein, although the contributions of these cells to demyelination are undefined [57].…”

Section: Jhmv-induced Demyelinationmentioning

confidence: 99%

CXCR2 Signaling and Host Defense Following Coronavirus-Induced Encephalomyelitis

2012

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Inoculation of the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the CNS of susceptible strains of mice results in widespread replication within glial cells, accompanied by infiltration of virus-specific T lymphocytes that control the virus through cytokine secretion and cytolytic activity. The virus persists within the 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. Shortly after JHMV infection, ELR-positive chemokines contribute to host defense by attracting CXCR2-expressing cells, including polymorphonuclear cells, to the CNS that aid host defense by increasing the permeability of the blood–brain barrier. 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 infection and highlights the different roles of CXCR2 signaling in these processes.

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Transcriptome profile within the mouse central nervous system and activation of myelin-reactive T cells following murine coronavirus infection

Cited by 11 publications

References 52 publications

Long-term human coronavirus-myelin cross-reactive T-cell clones derived from multiple sclerosis patients

Long-term human coronavirus-myelin cross-reactive T-cell clones derived from multiple sclerosis patients

Chemokine CXCL10 and Coronavirus-Induced Neurologic Disease

CXCR2 Signaling and Host Defense Following Coronavirus-Induced Encephalomyelitis

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