Mol Immunol. 2011 Jan;48(4):392-8. Epub 2010 Dec 4.

Recombinant YopJ induces apoptotic cell death in macrophages through TLR2.External

Pandey, A. K., Sodhi, A.,
--- - Faculty of Science, School of Biotechnology, Banaras Hindu University, Varanasi 221005, India.
Bacterial species evolved evasive maneuvers to bypass their recognition by the receptors primarily TLRs of the innate immune cells. We have reported that 3mug/ml of recombinant YopJ when provided extracellularly induced apoptosis in murine peritoneal macrophages in vitro. The present investigations demonstrate the role of TLR2 in apoptotic signals induced by rYopJ protein in murine peritoneal macrophages. The role of TLR2 in rYopJ induced macrophage apoptosis was shown by neutralization experiments and its co-immunoprecipitation with downstream molecule MyD88. The observed functional consequence of TLR2 neutralization were the inhibition of caspase-8 and caspase-3 activation, change in mitochondrial membrane potential (Deltapsim) and DNA fragmentation induced by rYopJ in macrophages. Further, rYopJ induced enhanced expression of IRAK-4, FADD, phosphorylation of IkappaB and p38 MAP kinase in macrophages. Pharmacological inhibitor of p38 MAP kinase and neutralization of TLR2 with neutralizing antibodies significantly inhibited the rYopJ induced caspases activation and DNA fragmentation, suggesting the possible involvement of TLR2 and p38 MAP kinase in rYopJ induced macrophages apoptosis.
PMID: 21131052External
Arrow2 In vitro interaction Arrow2 In vivo interaction Arrow2 Characterization Arrow2 Functional role Arrow2 top
In vivo interaction
Overexpression DD1 DD2 Reference
Family DD1 DD2 Method Species Region Species Region
DD FADD Link Myd88 Co-immunoprecipitation BALB/C Mouse peritoneal macrophage 21131052
(Link: click this icon to show interactions only between the two corresponding DDs)