TGF-β1 suppresses T cell infiltration and VP2 puff B mutation enhances apoptosis in acute polioencephalitis induced by Theiler's virus

Tsunoda, Ikuo; Libbey, Jane E.; Fujinami, Robert S.

doi:10.1016/j.jneuroim.2007.07.026

Cited by 20 publications

(30 citation statements)

References 58 publications

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“…The GDVII strain induced low numbers of infiltrating T cells in SJL/J mice but high levels of neuronal apoptosis, and there was a negative correlation between apoptosis and perivascular inflammation. The DApBL2M mutant induced high numbers of infiltrating T cells and high levels of neuronal apoptosis, and there was a positive correlation between apoptosis and perivascular inflammation (22). Here we found that in C57BL/6 mice the DApBL2M mutant induced the highest number of PVC, for those TMEVs compared, in infected mice developing seizures by day 7 p.i.…”

Section: Discussionsupporting

confidence: 53%

“…Differences in neuropathology during the acute phase in SJL/J mice have been described for the DA strain of the TO group, the GDVII strain of the GDVII group, and the DApBL2M mutant (22). The DA strain induced high numbers of infiltrating T cells (perivascular inflammation) in SJL/J mice but low levels of neuronal apoptosis, with no correlation be- tween the two.…”

Section: Discussionmentioning

confidence: 99%

“…The neuropathological changes observed in SJL/J mice during acute infection are distinct for the GDVII and DA strains (22). C57BL/6 mice infected i.c.…”

mentioning

confidence: 97%

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Lack of Correlation of Central Nervous System Inflammation and Neuropathology with the Development of Seizures following Acute Virus Infection

Libbey

Kennett

Wilcox

et al. 2011

J Virol

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

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Lack of Correlation of Central Nervous System Inflammation and Neuropathology with the Development of Seizures following Acute Virus Infection

Libbey

Kennett

Wilcox

et al. 2011

J Virol

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“…TMEV (86,96,97), porcine EMCV (17), and poliovirus (39) were reported to elicit apoptosis in certain cells of animals. It is not clear if these apoptotic events always developed as a direct consequence of viral reproduction in the target cells or if they were due to some secondary, e.g., immunological, reaction (52).…”

Section: Apoptosis-triggering and Apoptosis-preventing Functions Of Cmentioning

confidence: 99%

Antiapoptotic Activity of the Cardiovirus Leader Protein, a Viral “Security” Protein

Romanova

Lidsky

Kolesnikova

et al. 2009

J Virol

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Apoptosis is a common antiviral defensive mechanism that potentially limits viral reproduction and spread. Many viruses possess apoptosis-suppressing tools. Here, we show that the productive infection of HeLa cells with encephalomyocarditis virus (a cardiovirus) was not accompanied by full-fledged apoptosis (although the activation of caspases was detected late in infection) but rather elicited a strong antiapoptotic state, as evidenced by the resistance of infected cells to viral and nonviral apoptosis inducers. The development of the antiapoptotic state appeared to depend on a function(s) of the viral leader (L) protein, since its mutational inactivation resulted in the efflux of cytochrome c from mitochondria, the early activation of caspases, and the appearance of morphological and biochemical signs of apoptosis in a significant proportion of infected cells. Infection with both wild-type and L-deficient viruses induced the fragmentation of mitochondria, which in the former case was not accompanied with cytochrome c efflux. Although the exact nature of the antiapoptotic function(s) of cardioviruses remains obscure, our results suggested that it includes previously undescribed mechanisms operating upstream and possibly downstream of the mitochondrial level, and that L is involved in the control of these mechanisms. We propose that cardiovirus L belongs to a class of viral proteins, dubbed here security proteins, whose roles consist solely, or largely, in counteracting host antidefenses. Unrelated L proteins of other picornaviruses as well as their highly variable 2A proteins also may be security proteins. These proteins appear to be independent acquisitions in the evolution of picornaviruses, implying multiple cases of functional (though not structural) convergence.

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“…CD3 + T cells were visualized by antigen retrieval using citrate-based Vector ® Antigen Unmasking Solutions (Vector Laboratories, Burlingame, CA), followed by immunohistochemistry with anti-CD3 antibody (Dako, Carpinteria, CA), using the avidin-biotin-peroxidase complex (ABC) technique (Vector Laboratories) (42). The numbers of CD3 + cells were quantified under a light microscope using 10 to 12 transverse spinal cord segments per mouse as previously described (42).…”

Section: Methodsmentioning

confidence: 99%

Th17-biased RORγt transgenic mice become susceptible to a viral model for multiple sclerosis

Martinez

Sato

Kawai

et al. 2015

Brain, Behavior, and Immunity

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In a viral model for multiple sclerosis (MS), Theiler’s murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD), both immune-mediated tissue damage (immunopathology) and virus persistence have been shown to cause pathology. T helper (Th) 17 cells are a Th cell subset, whose differentiation requires the transcription factor retinoic acid-related orphan receptor (ROR) γt, secrete pro-inflammatory cytokines, including IL-17, and can antagonize Th1 cells. Although Th17 cells have been shown to play a pathogenic role in immune-mediated diseases or a protective role in bacterial and fungal infections, their role in viral infections is unclear. Using newly established Th17-biased RORγt Tg mice, we tested whether Th17 cells could play a pathogenic or protective role in TMEV-IDD by contributing to immunopathology and/or by modulating anti-viral Th1 immune responses. While TMEV-infected wild-type littermate C57BL/6 mice are resistant to TMEV-IDD, RORγt Tg mice developed inflammatory demyelinating lesions with virus persistence in the spinal cord. TMEV-infected RORγt Tg mice had higher levels of IL-17, lower levels of interferon-γ, and fewer CD8+ T cells, without alteration in overall levels of anti-viral lymphoproliferative and antibody responses, compared with TMEV-infected wild-type mice. This suggests that a Th17-biased “gain-of-function” mutation could increase susceptibility to virus-mediated demyelinating diseases.

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TGF-β1 suppresses T cell infiltration and VP2 puff B mutation enhances apoptosis in acute polioencephalitis induced by Theiler's virus

Cited by 20 publications

References 58 publications

Lack of Correlation of Central Nervous System Inflammation and Neuropathology with the Development of Seizures following Acute Virus Infection

Lack of Correlation of Central Nervous System Inflammation and Neuropathology with the Development of Seizures following Acute Virus Infection

Antiapoptotic Activity of the Cardiovirus Leader Protein, a Viral “Security” Protein

Th17-biased RORγt transgenic mice become susceptible to a viral model for multiple sclerosis

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