Activation of mouse liver natural killer cells and NK1.1+T cells by bacterial superantigen-primed Kupffer cells

Dobashi, Hiroshi; Seki, Shu; Habu, Yoshiko; Ohkawa, Taka-aki; Takeshita, Satoshi; Hiraide, Hoshio; Sekine, Isao

doi:10.1002/hep.510300209

Cited by 60 publications

(57 citation statements)

References 41 publications

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“…Kupffer cells can be activated by various bacterial stimuli and produce IL-12 and other cytokines (TNF-␣, IL-1␤, IL-18 etc. ), which are partly responsible for the activation of liver mononuclear cells (MNCs) (IFN-␥ production and cytotoxicity) (15,16). In this study, we demonstrate that the TLR9 ligand-primed liver is more sensitive to Con A-induced acute liver injury, and we investigate the underlying mechanisms of Kupffer cell dependence.…”

Section: Tlr-9 Activation Aggravates Concanavalin A-induced Hepatitismentioning

confidence: 86%

TLR-9 Activation Aggravates Concanavalin A-Induced Hepatitis via Promoting Accumulation and Activation of Liver CD4+ NKT Cells

Jiang

Sun

Zhou

et al. 2009

The Journal of Immunology

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Increasing evidence suggests that TLRs are involved in the pathogenesis of liver diseases; however, the underlying mechanisms remain obscure. In this study, we found that treatment with CpG-oligodeoxynucleotide (ODN) promoted the accumulation and activation of murine hepatic NKT cells. Additional experiments showed that CpG-ODN preferred to act on CD4+ NKT cells, while having less effect on CD4− NKT cells. The effect of CpG-ODN on liver NKT cells depended on the presence of Kupffer cells and IL-12. Meanwhile, CpG-ODN pretreatment aggravated liver injury and promoted the production of inflammatory cytokines in a Con A-induced fulminant hepatitis model via TLR9 activation. Collectively, our data demonstrate that TLR9 stimulation prefers to promote the accumulation and activation of hepatic CD4+ NKT cells and suggest that TLR9 signaling might be involved in the pathogenesis of human hepatitis.

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Section: Tlr-9 Activation Aggravates Concanavalin A-induced Hepatitismentioning

confidence: 86%

TLR-9 Activation Aggravates Concanavalin A-Induced Hepatitis via Promoting Accumulation and Activation of Liver CD4+ NKT Cells

Jiang

Sun

Zhou

et al. 2009

The Journal of Immunology

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“…The first link of this toxin with NK cells was probably reported in 1991 by Sacks et al (49), who showed that SPEA increased NK cell cytotoxic activity. The capacity of SPEA to activate NK cells and induce IFN-γ was further confirmed (50). Staphylococcal enterotoxin B is another superantigen able to induce the release of IFN-γ by purified NK cells (51).…”

Section: Bacterial Sensing By Nk Cells and Expression Of Prrsmentioning

confidence: 88%

Natural Killer (NK) Cells in Antibacterial Innate Immunity: Angels or Devils?

Souza-Fonseca-Guimarães

Adib‐Conquy

Cavaillon

2011

Mol Med

134

125

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Natural killer (NK) cells were first described as immune leukocytes that could kill tumor cells and soon after were reported to kill virus-infected cells. In the mid-1980s, 10 years after their discovery, NK cells were also demonstrated to contribute to the fight against bacterial infection, particularly because of crosstalk with other leukocytes. A wide variety of immune cells are now recognized to interact with NK cells through the production of cytokines such as interleukin (IL)-2, IL-12, IL-15 and IL-18, which boost NK cell activities. The recent demonstration that NK cells express pattern recognition receptors, namely Toll-like and nucleotide oligomerization domain (NOD)-like receptors, led to the understanding that these cells are not only under the control of accessory cells, but can be directly involved in the antibacterial response thanks to their capacity to recognize pathogen-associated molecular patterns. Interferon (IFN)-γ is the predominant cytokine produced by activated NK cells. IFN-γ is a key contributor to antibacterial immune defense. However, in synergy with other inflammatory cytokines, IFN-γ can also lead to deleterious effects similar to those observed during sepsis. Accordingly, as the main source of IFN-γ in the early phase of infection, NK cells display both beneficial and deleterious effects, depending on the circumstances.

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“…The liver MNC were prepared essentially as previously described [21,45,46]. Briefly, the livers were minced and suspended in HBSS containing 0.05% collagenase (Wako, Osaka, Japan), and then were shaken for 20 min in a 37 C water bath.…”

Section: Isolation Of Mnc or Kupffer Cellsmentioning

confidence: 99%

Critical role of the liver CD8⁺ CD122⁺ T cells in the generalized Shwartzman reaction of mice

et al. 2005

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We examined the role of mouse CD8+ CD122+ T cells, which increase in number with age, in the generalized Shwartzman reaction. This reaction was induced by IL‐12 priming and subsequent LPS challenge (after 24 h) in mice of various ages (4–50 weeks of age). Although most young mice (4 or 6 weeks of age) survived, mortality essentially increased with increasing age of the mice, and all mice of 20 weeks of age or older died within 48 h. Serum TNF‐α levels after LPS challenge also increased age dependently. The neutralization of either IL‐12‐induced IFN‐γ or LPS‐induced TNF‐α improved the survival of middle‐aged (25‐week‐old) mice. Both IFN‐γ production after IL‐12 priming and TNF‐α production from the liver mononuclear cells after LPS challenge were also prominent in the middle‐aged mice. CD8+CD122+ T cells cultured with IL‐12 produced a much larger amount of IFN‐γ than CD8+CD122– T cells. Although the depletion of NK/NK T cells did not decrease the IFN‐γ or TNF‐α production in the Shwartzman reaction of the middle‐aged mice, an additional depletion of CD8+CD122+ T cells did decrease such production and also improved mouse survival. Furthermore, young mice transferred with CD8+CD122+ T cells from aged B6 nude mice showed an enhanced Shwartzman reaction.

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Activation of mouse liver natural killer cells and NK1.1+T cells by bacterial superantigen-primed Kupffer cells

Cited by 60 publications

References 41 publications

TLR-9 Activation Aggravates Concanavalin A-Induced Hepatitis via Promoting Accumulation and Activation of Liver CD4+ NKT Cells

TLR-9 Activation Aggravates Concanavalin A-Induced Hepatitis via Promoting Accumulation and Activation of Liver CD4+ NKT Cells

Natural Killer (NK) Cells in Antibacterial Innate Immunity: Angels or Devils?

Critical role of the liver CD8⁺ CD122⁺ T cells in the generalized Shwartzman reaction of mice

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Activation of mouse liver natural killer cells and NK1.1+T cells by bacterial superantigen-primed Kupffer cells

Cited by 60 publications

References 41 publications

TLR-9 Activation Aggravates Concanavalin A-Induced Hepatitis via Promoting Accumulation and Activation of Liver CD4+ NKT Cells

TLR-9 Activation Aggravates Concanavalin A-Induced Hepatitis via Promoting Accumulation and Activation of Liver CD4+ NKT Cells

Natural Killer (NK) Cells in Antibacterial Innate Immunity: Angels or Devils?

Critical role of the liver CD8+ CD122+ T cells in the generalized Shwartzman reaction of mice

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Product

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Critical role of the liver CD8⁺ CD122⁺ T cells in the generalized Shwartzman reaction of mice