IL-12, while beneficial, is not essential for the host response to VSV encephalitis

David A. Chesler, Carol Reiss

Research output: Contribution to journalArticle

Abstract

In this report, the role of STAT4 and local production of interleukin (IL)-12 in the central nervous system (CNS) were examined during experimental vesicular stomatitis virus (VSV) encephalitis. We have previously shown that IL-12 treatment is beneficial both in vitro and in vivo during experimental VSV infection. This inhibition of VSV replication was dependent on the production of nitric oxide (NO) by the neuronal isoform of nitric oxide synthase (NOS-1). In vitro, IL-12 induces the phosphorylation and nuclear localization of STAT4 in neuroblastoma cell lines. STAT4 expression was not required for host survival or clearance of virus during experimental VSV encephalitis. Taken together, these data suggest that while neurons can respond directly to IL-12 in vitro by signaling through STAT4, STAT4 is not required for survival. It is likely that redundant innate host inflammatory cytokine responses compensate for the absence of IL-12 signaling.

Original languageEnglish (US)
Pages (from-to)92-97
Number of pages6
JournalJournal of Neuroimmunology
Volume131
Issue number1-2
DOIs
StatePublished - Oct 2002

Fingerprint

Encephalitis Viruses
Vesicular Stomatitis
Interleukin-12
Nitric Oxide Synthase Type I
Virus Diseases
Virus Replication
Neuroblastoma
Nitric Oxide
Protein Isoforms
Central Nervous System
Phosphorylation
Cytokines
Viruses
Neurons
Cell Line
In Vitro Techniques

Keywords

  • Host response
  • IL-12
  • VSV

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

Cite this

IL-12, while beneficial, is not essential for the host response to VSV encephalitis. / Chesler, David A.; Reiss, Carol.

In: Journal of Neuroimmunology, Vol. 131, No. 1-2, 10.2002, p. 92-97.

Research output: Contribution to journalArticle

@article{23717ff80dc347e5b779054f8096555a,
title = "IL-12, while beneficial, is not essential for the host response to VSV encephalitis",
abstract = "In this report, the role of STAT4 and local production of interleukin (IL)-12 in the central nervous system (CNS) were examined during experimental vesicular stomatitis virus (VSV) encephalitis. We have previously shown that IL-12 treatment is beneficial both in vitro and in vivo during experimental VSV infection. This inhibition of VSV replication was dependent on the production of nitric oxide (NO) by the neuronal isoform of nitric oxide synthase (NOS-1). In vitro, IL-12 induces the phosphorylation and nuclear localization of STAT4 in neuroblastoma cell lines. STAT4 expression was not required for host survival or clearance of virus during experimental VSV encephalitis. Taken together, these data suggest that while neurons can respond directly to IL-12 in vitro by signaling through STAT4, STAT4 is not required for survival. It is likely that redundant innate host inflammatory cytokine responses compensate for the absence of IL-12 signaling.",
keywords = "Host response, IL-12, VSV",
author = "Chesler, {David A.} and Carol Reiss",
year = "2002",
month = "10",
doi = "10.1016/S0165-5728(02)00257-6",
language = "English (US)",
volume = "131",
pages = "92--97",
journal = "Journal of Neuroimmunology",
issn = "0165-5728",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - IL-12, while beneficial, is not essential for the host response to VSV encephalitis

AU - Chesler, David A.

AU - Reiss, Carol

PY - 2002/10

Y1 - 2002/10

N2 - In this report, the role of STAT4 and local production of interleukin (IL)-12 in the central nervous system (CNS) were examined during experimental vesicular stomatitis virus (VSV) encephalitis. We have previously shown that IL-12 treatment is beneficial both in vitro and in vivo during experimental VSV infection. This inhibition of VSV replication was dependent on the production of nitric oxide (NO) by the neuronal isoform of nitric oxide synthase (NOS-1). In vitro, IL-12 induces the phosphorylation and nuclear localization of STAT4 in neuroblastoma cell lines. STAT4 expression was not required for host survival or clearance of virus during experimental VSV encephalitis. Taken together, these data suggest that while neurons can respond directly to IL-12 in vitro by signaling through STAT4, STAT4 is not required for survival. It is likely that redundant innate host inflammatory cytokine responses compensate for the absence of IL-12 signaling.

AB - In this report, the role of STAT4 and local production of interleukin (IL)-12 in the central nervous system (CNS) were examined during experimental vesicular stomatitis virus (VSV) encephalitis. We have previously shown that IL-12 treatment is beneficial both in vitro and in vivo during experimental VSV infection. This inhibition of VSV replication was dependent on the production of nitric oxide (NO) by the neuronal isoform of nitric oxide synthase (NOS-1). In vitro, IL-12 induces the phosphorylation and nuclear localization of STAT4 in neuroblastoma cell lines. STAT4 expression was not required for host survival or clearance of virus during experimental VSV encephalitis. Taken together, these data suggest that while neurons can respond directly to IL-12 in vitro by signaling through STAT4, STAT4 is not required for survival. It is likely that redundant innate host inflammatory cytokine responses compensate for the absence of IL-12 signaling.

KW - Host response

KW - IL-12

KW - VSV

UR - http://www.scopus.com/inward/record.url?scp=0036789959&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036789959&partnerID=8YFLogxK

U2 - 10.1016/S0165-5728(02)00257-6

DO - 10.1016/S0165-5728(02)00257-6

M3 - Article

VL - 131

SP - 92

EP - 97

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

SN - 0165-5728

IS - 1-2

ER -