TLR2 Modulates Antibodies Required for Intestinal Ischemia/Reperfusion-Induced Damage and Inflammation

摘要: In multiple clinical conditions, including trauma and hemorrhage, reperfusion magnifies ischemic tissue damage. Ischemia induces expression of neoantigens, lipid alterations that are recognized by the serum protein, β2-glycoprotein I (β2-GPI). During reperfusion, binding β2-GPI naturally occurring Abs results in an excessive inflammatory response may lead to death. As is critical for intestinal ischemia/reperfusion (IR)-induced damage TLR2 one proposed receptors β2-GPI, we hypothesized IR-induced inflammation require TLR2. Using TLR2(-/-) mice, demonstrate required mucosal damage, as well complement activation proinflammatory cytokine production. IR, mice have increased compared with wild-type but not deposited on tissue. addition, also did express other novel Ags, suggesting a sequential response. Unlike TLRs, lacked appropriate Ab repertoire induce IR or inflammation. Together, these data suggest that, addition response, injury requires