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The IL-12 response to herpes simplex virus is mainly a paracrine response of reactive inflammatory cells.
- Source :
-
Journal of leukocyte biology [J Leukoc Biol] 2002 Sep; Vol. 72 (3), pp. 564-70. - Publication Year :
- 2002
-
Abstract
- 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.
- Subjects :
- Animals
Cell Line metabolism
Cornea cytology
Cornea virology
Cycloheximide pharmacology
Defective Viruses physiology
Epithelial Cells virology
Interleukin-12 genetics
Keratitis, Herpetic
Mice
Mice, Inbred BALB C
Organ Specificity
Protein Synthesis Inhibitors pharmacology
Simplexvirus genetics
Simplexvirus radiation effects
Viral Proteins biosynthesis
Virus Replication
Interleukin-12 biosynthesis
Macrophages, Peritoneal metabolism
Paracrine Communication physiology
Simplexvirus physiology
T-Lymphocytes metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0741-5400
- Volume :
- 72
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Journal of leukocyte biology
- Publication Type :
- Academic Journal
- Accession number :
- 12223525