Genetic background influences natural killer cell activation during bacterial peritonitis in mice, and is interleukin 12 and interleukin 18 independent.

Abstract

Some mouse strains produce strong pro-inflammatory, T-helper (Th)1 responses (e.g. C57BL/6), or strong anti-inflammatory, Th2 responses (e.g. BALB/c). The exact mechanisms for development of distinct immune responses to infection are not completely understood, although cytokines such as interleukin (IL)-12, IL-18 and IL-4 are known to play roles. Natural killer T (NKT)/natural killer (NK) cells are important regulators of immune responses in infection and non-infection models, and NKT/NK activation is also regulated by IL-12 and IL-18 in many models. We investigated the role of IL-12/IL-18 in NKT/NK activation in murine bacterial peritonitis, as well as differential NKT and NK cell activation in C57BL/6 and BALB/c mice. No differences in NKT or NK cell activation or intracellular interferon (IFN)-gamma were determined between mice given control, anti-IL-12 or anti-IL-18 antibodies or in NKT/NK cell activation in STAT4-/- mice (deficient in IL-12 signaling) or wild type controls. However, there were significant differences in the activation of NKT and NK cells between C57BL/6 mice and BALB/c mice, with NKT/NK cytokine production following Th1 or Th2 lines dependent on strain. This suggests a role for NKT and NK cell activation in the development of Th1 and Th2 responses during bacterial infection independently of IL-12 or IL-18.

• Authors: Melanie J Scott, J Jason Hoth, Sarah A Gardner, James C Peyton, William G Cheadle
• Journal: Cytokine (Cytokine) Vol. 28 Issue 3 Pg. 124-36 (Nov 07 2004) ISSN: 1043-4666 [Print] England
• PMID: 15473954 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S.)

Chemical References

• Antibodies
• Cytokines
• DNA-Binding Proteins
• Interleukin-18
• STAT4 Transcription Factor
• Stat4 protein, mouse
• Trans-Activators
• Interleukin-12
• Interferon-gamma

Topics

• Animals
• Antibodies (immunology, pharmacology)
• Bacterial Infections (genetics, immunology)
• Cytokines (metabolism)
• DNA-Binding Proteins (deficiency, genetics, metabolism)
• Interferon-gamma (metabolism)
• Interleukin-12 (immunology, metabolism)
• Interleukin-18 (immunology, metabolism)
• Killer Cells, Natural (cytology, immunology)
• Lymphocyte Activation
• Mice
• Mice, Inbred BALB C
• Mice, Inbred C57BL
• Mice, Knockout
• Neutralization Tests
• Peritonitis (genetics, immunology)
• STAT4 Transcription Factor
• Spleen (immunology, metabolism)
• Survival Rate
• Trans-Activators (deficiency, genetics, metabolism)