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.

journal_name

J Neuroimmunol

authors

Chesler DA,Reiss CS

doi

10.1016/s0165-5728(02)00257-6

subject

Has Abstract

pub_date

2002-10-01 00:00:00

pages

92-7

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165572802002576

journal_volume

131

pub_type

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