Absence of SHIP-1 results in constitutive phosphorylation of tank-binding kinase 1 and enhanced TLR3-dependent IFN-beta production.

@article{Gabhann2010AbsenceOS,
  title={Absence of SHIP-1 results in constitutive phosphorylation of tank-binding kinase 1 and enhanced TLR3-dependent IFN-beta production.},
  author={Joan N{\'i} Gabhann and Rowan Higgs and Kiva Brennan and Warren Thomas and Jacqueline E. Damen and Nadia Ben Larbi and Gerald Krystal and Caroline A. Jefferies},
  journal={Journal of immunology},
  year={2010},
  volume={184 5},
  pages={2314-20}
}
Autoimmune diseases, such as systemic lupus erythematosus and rheumatoid arthritis, result from a loss of tolerance to self-antigens and immune-mediated injury precipitated by the overproduction of type I IFN and inflammatory cytokines. We have identified the inositol 5' phosphatase SHIP-1 as a negative regulator of TLR3-induced type I IFN production. SHIP-1-deficient macrophages display enhanced TLR-induced IFN-beta production, and overexpression of SHIP-1 negatively regulates the ability of… CONTINUE READING

Citations

Publications citing this paper.
Showing 1-10 of 38 extracted citations

References

Publications referenced by this paper.
Showing 1-10 of 55 references

Similar Papers

Loading similar papers…