title: Infectious tolerance to ADP/ATP carrier peptides induced by anti-L3T4 monoclonal antibody in dilated cardiomyopathy mice.
abstract: CD4 T cells are suspected to play an important role in the pathogenesis of dilated cardiomyopathy (DCM). This study sought to evaluate whether anti-L3T4 monoclonal antibody (McAb) could induce the infectious tolerance to the adenosine diphosphate (ADP)/adenosine triphosphate (ATP) carrier peptides to protect mice from DCM. BALB/c mice (n = 16) were immunized with the peptides derived from human ADP/ATP carrier on the 1st, 14th, 28th, 49th, and 79th days, and some of them (n = 6) were also injected with anti-L3T4 McAb on the -1st, 0, and 1st days. On the 180th day, the splenocytes (SC) from the McAb-treated group were transferred into the syngeneic recipients (n = 6) who were also immunized with the peptides in the same manner. The sham-immunized mice were taken as the controls (n = 10). Results showed that the serum antibody against the ADP/ATP carrier examined with ELISA was positive in all mice only immunized with the peptides (DCM group), while negative in the McAb-treated, the SC-transferred, and the Control groups. The mRNA expression of IFN-gamma, IL-2, and IL-4, especially IL-4 in T cells investigated using real-time quantitative PCR and the percentages of T helper 1 (Th1) and Th2 subsets, especially Th2 subset detected with Flow Cytometry were all increased in DCM group, accompanied by the cardiac histopathological changes like those in DCM. Such findings were not seen in the other three groups. It concluded that anti-L3T4 McAb could inhibit the occurrence of DCM induced by the ADP/ATP carrier peptides in mice, and this immune tolerance could be transferred to the syngeneic recipients.
authors.affiliation: Institute of Cardiovascular diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. liaoyh27@hotmail.com
authors.forename: Yu-Hua
authors.initials: YH
authors.lastname: Liao
authors.forename: Jing
authors.initials: J
authors.lastname: Yuan
authors.forename: Zhao-Hui
authors.initials: ZH
authors.lastname: Wang
authors.forename: Xiang
authors.initials: X
authors.lastname: Cheng
authors.forename: Jing-Hui
authors.initials: JH
authors.lastname: Zhang
authors.forename: Yuan
authors.initials: Y
authors.lastname: Tian
authors.forename: Ji-Hua
authors.initials: JH
authors.lastname: Dong
authors.forename: He-Ping
authors.initials: HP
authors.lastname: Guo
authors.forename: Min
authors.initials: M
authors.lastname: Wang
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D015704:CD4 Antigens / Q000276:immunology*; D002311:Cardiomyopathy, Dilated / Q000201:enzymology* / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology*; D017710:Lymphocyte Transfusion; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D000226:Mitochondrial ADP, ATP Translocases / Q000276:immunology*; D010455:Peptides / Q000008:administration & dosage* / Q000138:chemical synthesis / Q000276:immunology*; D013154:Spleen / Q000166:cytology / Q000276:immunology / Q000637:transplantation; D013601:T-Lymphocytes / Q000201:enzymology / Q000276:immunology / Q000637:transplantation; D018417:Th1 Cells / Q000201:enzymology / Q000276:immunology / Q000637:transplantation; D018418:Th2 Cells / Q000201:enzymology / Q000276:immunology / Q000637:transplantation
chemical_list: D000911:Antibodies, Monoclonal; D015704:CD4 Antigens; D016207:Cytokines; D010455:Peptides; D000226:Mitochondrial ADP, ATP Translocases