Open AccessThe complement dependent cytotoxicity (CDC) immune effector mechanism contributes to anti-CD154 induced immunosuppression.
Author(s) -
Alberto SánchezFueyo,
Christoph Domenig,
Terry B. Strom,
Xin Xiao Zheng
Publication year - 2002
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/00007890-200209270-00031
Subject(s) - cd154 , complement dependent cytotoxicity , cd40 , immunosuppression , immune tolerance , immunology , monoclonal antibody , islet , transplantation , immune system , medicine , biology , cytotoxic t cell , antibody , antibody dependent cell mediated cytotoxicity , endocrinology , in vitro , diabetes mellitus , biochemistry
In many situations, anti-CD154 (CD40 ligand) monoclonal antibody (mAb) treatment is very potent in producing allograft tolerance. In accordance to our previously reported results, combined donor specific transfusion (DST)3 plus anti-CD154 mAb (MR1) treatment enables the permanent engraftment of DBA/2 (H-2(d)) islets into B6AF1 (H-2(b/kd)) recipients in all cases. It has been widely assumed that the MR1 anti-154 is a noncytolytic neutralizing mAb, and it exerts immune suppressive effects by blockade of CD40/CD154 signal pathway. In this study, we sought to test the role of complement dependent cytotoxicity (CDC) immune effector mechanism in MR1 anti-CD154 induced immunosuppression.