Premium
The IL‐12 response to herpes simplex virus is mainly a paracrine response of reactive inflammatory cells
Author(s) -
Kumaraguru Udayasankar,
Rouse B. T.
Publication year - 2002
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.72.3.564
Subject(s) - herpes simplex virus , biology , paracrine signalling , cytokine , hsl and hsv , virus , immunology , inflammation , virology , viral replication , receptor , biochemistry
Herpes simplex virus (HSV) infection results in rapid and sustained up‐regulation of interleukin (IL)‐12, but the primary cellular source of IL‐12 after HSV infection is unknown. We demonstrate that this cytokine largely derives from inflammatory cells rather than from productively infected epithelial cells. For optimal IL‐12 induction, epithelial cells needed to be infected with replication‐competent virus, and cells needed to be able to synthesize proteins. Our results also indicate that HSV‐infected cells generate intermediary products that signal recruited inflammatory cells, which themselves were not HSV‐infected, to generate IL‐12. Possible mechanisms by which infected cells communicate with inflammatory cells to cause IL‐12 production are discussed.