Role of PKC isoforms in the FcγR‐mediated inhibition of LPS‐stimulated IL‐12 secretion by macrophages

@article{Fronhofer2006RoleOP,
  title={Role of PKC isoforms in the Fc$\gamma$R‐mediated inhibition of LPS‐stimulated IL‐12 secretion by macrophages},
  author={Van Fronhofer and Michelle R. Lennartz and Daniel J. Loegering},
  journal={Journal of Leukocyte Biology},
  year={2006},
  volume={79}
}
Ligation of Fc receptors for immunoglobulin G (FcγRs) inhibits lipopolysaccharide (LPS)‐stimulated secretion of interleukin (IL)‐12 by macrophages. FcγR activation of protein kinase C (PKC) contributes to several functions of this receptor including phagocytosis, activation of the reduced nicotinamide adenine dinucleotide phosphate oxidase, and secretion of certain cytokines. Therefore, we tested the hypothesis that PKC mediates the FcγR inhibition of IL‐12 secretion by macrophages. In murine… 

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References

SHOWING 1-10 OF 49 REFERENCES

Critical role of protein kinase C ϵ for lipopolysaccharide‐induced IL‐12 synthesis in monocyte‐derived dendritic cells

Evidence that PKC inhibition impairs LPS signaling in DC is provided and PKC ϵ is identified as a potential target for the inhibition of Toll‐like receptor‐4‐mediated, IL‐12‐dependent Th1 type responses is identified.

Differential regulation of monocytic tumor necrosis factor‐α and interleukin‐10 expression

It is shown that the regulation of IL‐10 expression is more complex than that of TNF‐α, and the modulation of IL-10 expression by inflammatory mediators suggests a regulatory circuit of the inflammatory response.

HIV‐1 Tat protein induces interleukin‐10 in human peripheral blood monocytes: involvement of protein kinase C‐βII and ‐δ

The results suggest that the induction of IL‐10 by Tat is strictly dependent on the PKC‐δ and ‐βII isoforms.

Immune complexes are potent inhibitors of interleukin‐12 secretion by human monocytes

It is concluded that IC, typically appearing in the course of chronic inflammatory processes, may influence the balance between Th1 and Th2 responses and may thus contribute to a deprivation of cell‐mediated immune responses.

Signaling Pathways for Fcγ Receptor-Stimulated Tumor Necrosis Factor-α Secretion and Respiratory Burst in RAW 264.7 Macrophages

Interferon-γ treated RAW 264.7 cells are a model of inflammatory macrophages and well suited for further study of these signaling pathways, which mediates several important macrophage functions including cytokine secretion and respiratory burst.

Selective Suppression of Interleukin-12 Induction after Macrophage Receptor Ligation

The results indicate that the calcium influxes that occur as a result of receptor ligation are responsible for inhibiting the induction of IL-12 by LPS, which may be a way of limiting proinflammatory responses of macrophages to extracellular pathogens, or suppressing the development of cell-mediated immunity to intracellular pathogens.

Signaling by IL‐12 and IL‐23 and the immunoregulatory roles of STAT4

Summary:  Produced in response to a variety of pathogenic organisms, interleukin (IL)‐12 and IL‐23 are key immunoregulatory cytokines that coordinate innate and adaptive immune responses. These

Interleukin‐12 is required for interferon‐γ production and lethality in lipopolysaccharide‐induced shock in mice

IL‐12 is required for IFN‐γ production and lethality in an endotoxic shock model in mice because co‐injection of TNF‐α and IL‐12, sufficient to induce serum concentrations of both cytokines higher and more persistent than those obtained by injection of LPS, was not sufficient to induced IFN-γ production in vivo.

Reversal of Proinflammatory Responses by Ligating the Macrophage Fcγ Receptor Type I

It is demonstrated that ligation of macrophage Fcγ receptors (FcγR) can lead to a reversal ofmacrophage proinflammatory responses by inducing an upregulation of interleukin (IL)-10, with a reciprocal inhibition of IL-12 production.