Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Reperfusion of ischemic tissues elicits an acute inflammatory response involving serum complement, which is activated by circulating natural IgM specific to self-Ags exposed by ischemia. Recent reports demonstrating a role for the lectin pathway raise a question regarding the initial events in complement activation. To dissect the individual roles of natural IgM and lectin in activation of complement, mice bearing genetic deficiency in early complement, IgM, or mannan-binding lectin were characterized in a mesenteric model of ischemia reperfusion injury. The results reveal that IgM binds initially to ischemic Ag providing a binding site for mannan-binding lectin which subsequently leads to activation of complement and injury.

Type

Journal article

Journal

J Immunol

Publication Date

01/10/2006

Volume

177

Pages

4727 - 4734

Keywords

Amino Acid Sequence, Animals, Antigen-Antibody Complex, Autoantigens, Complement Pathway, Mannose-Binding Lectin, Disease Models, Animal, Immunoglobulin M, Immunohistochemistry, Immunoprecipitation, Inflammation, Mannose-Binding Lectin, Mass Spectrometry, Mesentery, Mice, Mice, Inbred C57BL, Mice, Knockout, Molecular Sequence Data, Myosin Heavy Chains, Myosin Type II, Reperfusion Injury