The IL-12 response to herpes simplex virus is mainly a paracrine response of reactive inflammatory cells.
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.
Kumaraguru
Udayasankar
U
Department of Microbiology, University of Tennessee, Knoxville 37996, USA.
Rouse
B T
BT
D000818:Animals; D002460:Cell Line / Q000378:metabolism; D003315:Cornea / Q000166:cytology / Q000821:virology; D003513:Cycloheximide / Q000494:pharmacology; D003673:Defective Viruses / Q000502:physiology; D004847:Epithelial Cells / Q000821:virology; D018664:Interleukin-12 / Q000096:biosynthesis* / Q000235:genetics; D016849:Keratitis, Herpetic; D017737:Macrophages, Peritoneal / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D009928:Organ Specificity; D019899:Paracrine Communication / Q000502:physiology*; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D018139:Simplexvirus / Q000235:genetics / Q000502:physiology* / Q000528:radiation effects; D013601:T-Lymphocytes / Q000378:metabolism*; D014764:Viral Proteins / Q000096:biosynthesis; D014779:Virus Replication
D011500:Protein Synthesis Inhibitors; D014764:Viral Proteins; D018664:Interleukin-12; D003513:Cycloheximide