Interleukin-12 protects thermally injured mice from herpes simplex virus type 1 infection

Ryuichi Matsuo, Makiko Kobayashi, David N. Herndon, Richard B Pollard, Fujio Suzuki

Research output: Contribution to journalArticle

54 Scopus citations

Abstract

Severe burn injury is associated with increased susceptibility to severe herpesvirus infections. Type 2 cytokines [interleukin (IL)-4 and IL-10] released from burn-associated CD8+ type 2 T cells (BA-type 2 T cells) have been shown to play a role in the increased susceptibility of thermally injured mice (TI-mice) to herpes simplex virus type 1 (HSV-1) infection. Because IL-12 has been shown to inhibit the generation of type 2 T cells, murine rIL-12 was injected into TI-mice exposed to HSV-1 to determine whether IL-12 could influence HSV-1 infections in individuals bearing type 2 T cells. rIL-12 improved the resistance of TI-mice or mice inoculated with T6S cells (a BA-type 2 T cell clone) against HSV-1 infection. Type 2 cytokines were detected in sera of TI-mice or mice inoculated with T6S cells (T6S-mice). However, treatment of TI-mice or T6S-mice with rIL-12 inhibited type 2 cytokine production in the sera of these mice. All TI-mice exposed to a lethal dose of HSV-1 survived when they were treated with a mixture of monoclonal antibodies (mbs) against type 2 cytokines. Staphylococcal enterotoxin A [an interferon-γ (IFN-γ) inducer] stimulated serum IFN-γ production in TI-mice and T6S-mice treated with rIL-12, whereas no IFN-γ was produced in mice treated with saline. These results suggest that IL-12 has the potential to protect TI-mice infected with a lethal dose of HSV-1 via a shift to type 1 T cell responses from type 2 T cell responses.

Original languageEnglish (US)
Pages (from-to)623-630
Number of pages8
JournalJournal of Leukocyte Biology
Volume59
Issue number5
StatePublished - May 1996
Externally publishedYes

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Keywords

  • interferon- γ
  • interleukin-4
  • type 1 T cell responses
  • type 2 T cell responses

ASJC Scopus subject areas

  • Cell Biology

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