• Nenhum resultado encontrado

Distinct dictation of Japanese encephalitis virus-induced neuroinflammation and lethality via triggering TLR3 and TLR4 signal pathways.

N/A
N/A
Protected

Academic year: 2017

Share "Distinct dictation of Japanese encephalitis virus-induced neuroinflammation and lethality via triggering TLR3 and TLR4 signal pathways."

Copied!
21
0
0

Texto

Loading

Imagem

Figure 2. Enhanced inflammation of the CNS in TLR3 2/2 mice following JEV infection. A and B
Figure 4. BBB permeability is increased after JEV infection in TLR3 2/2 but not TLR4 2/2 mice
Figure 5. The spread of JEV in the brain of TLR3 2/2 and TLR4 2/2 mice after intracranial inoculation
Figure 7. Virus control and type I IFN responses of myeloid cells derived from TLR3 2/2 and TLR4 2/2 mice to JEV infection
+3

Referências

Documentos relacionados

amazonensis.29 This protection is associated with the development of a Thl type response as measured by increased IFN-r and lack of IL-4 production by spleen

We show that (1) mRNAs of type I IFN family members are up-regulated in lesional skin but not in nonlesional skin (except IFN- a 5 and IFN- k ); (2) IFN- a / b signaling pathway is

Similarly, it has been demonstrated that whole cell pertussis vaccine immunization led to comparable antibody titers in TLR4-deficient and wild type mice, but IFN- c and

Next, to determine what ligand stimuli could induce potent type I IFN production in pso- riasis patients by RIG-I dependent manner, we isolated three psoriasis patients ’ PBMCs

The major findings in the present study are that: 1) endogenous type I IFN-like activity and treatment with IFN- b are both associated with reduced expression of CD49d on CD26 high

In the absence of type I and II IFN receptors or the transcription factor STAT1, suckling mice are deficient in IFN signaling and become much more susceptible to heterologous, but

We have shown for the first time that HSV-2 activates TLR4- dependent NF-kB activation and TLR4-dependent Mal/MyD88/ NF-kB signaling contributes to the innate immune response in

Hence, to generalize our observation that very low levels of IFN-I production are sufficient to induce strong IFN-I responses, we next measured pangenomic ISG induction in mice with