Assessment of ¹⁸⁸Re marked anti MHC class II antibody by peripheral blood mononuclear cells stimulated by donor alloantigen.
- Author:
Guo-Ping DING
1
;
Li-Ping CAO
;
Jie LIU
;
Da-Ren LIU
;
Ri-Sheng QUE
;
Lin-Hua ZHU
;
Yi-Ming ZHOU
;
Ke-Jie MAO
;
Jun-An HU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antibodies, Monoclonal; chemistry; pharmacology; Cell Proliferation; drug effects; Interleukin-10; genetics; Interleukin-2; genetics; Isoantigens; immunology; Leukocytes, Mononuclear; drug effects; radiation effects; Lymphocyte Culture Test, Mixed; Mitomycin; pharmacology; Radioisotopes; Reverse Transcriptase Polymerase Chain Reaction; Rhenium; Swine; Tumor Necrosis Factor-alpha; genetics
- From: Chinese Medical Journal 2011;124(16):2512-2516
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDPrevious studies showed that anti MHC-II monoclone antibody (MAb) only had partial inhibiting effect of alloreactive mixed lymphocyte reaction (MLR) in vitro and it was unsteady and non-persistent. The aim of this research was to determine whether radioactive isotope (188)Re marked MHC-II antibody could benefit the allograft acceptance in transplantation as compared to normal MHC-II antibody.
METHODS188Re was incorporated to 2E9/13F (ab')(2) which is against swine MHC class II antigen (MAb-(188)Re). Porcine peripheral blood mononuclear (PBMC) cells were examined for proliferation and cytokine mRNA expression after stimulation with MHC-II MAb or MAb-(188)Re.
RESULTSThe proliferative response of recipient PBMCs in mixed lymphocyte reaction (MLR) to donor alloantigen showed that the stimulation index of MAb-(188)Re group was significantly lower than the MHC-II MAb group and control (P < 0.05). mRNA expression of interleukin 2, interferon Υ and tumor necrosis factor α (type 1 cytokines) was lower in MAb-(188)Re group than the MHC-II MAb group, while interleukin 10 (type 2 cytokines) was higher in MAb-(188)Re group in the first 24 hours.
CONCLUSIONMAb-(188)Re could help the graft acceptance by inhibiting T cell proliferation, lowering the expression of type 1 cytokines and elevating the type 2 cytokines produced by PBMC.
