Effects of humanized recombinant CD25 monoclonal antibody on activation and proliferation of t lymphocytes.
- Author:
Wei LIU
1
;
Han-Yun REN
Author Information
1. Department of Hematology, The First Hospital, Peking University, Beijing 100034, China.
- Publication Type:Journal Article
- MeSH:
Antibodies, Monoclonal;
pharmacology;
CD3 Complex;
biosynthesis;
genetics;
Cell Proliferation;
Cells, Cultured;
Cyclosporine;
pharmacology;
Humans;
Immunosuppressive Agents;
pharmacology;
Interleukin-2 Receptor alpha Subunit;
biosynthesis;
genetics;
immunology;
Lymphocyte Activation;
immunology;
Receptors, Interleukin-2;
analysis;
Recombinant Proteins;
immunology;
pharmacology;
T-Lymphocytes;
immunology
- From:
Journal of Experimental Hematology
2007;15(1):134-137
- CountryChina
- Language:Chinese
-
Abstract:
The study was purposed to investigate the effects of humanized recombined CD25 monoclonal antibody (rhCD25MAb) on activation and proliferation of T lymphocytes in vitro. Peripheral blood mononuclear cells (PBMNC) were incubated with phytohemagglutinin (PHA). Before or after T cell activation, the cells were cultured with or without rhCD25MAb or cyclosporine A (CsA) in vitro. After 72 hours incubation, the proliferation of lymphocytes was analyzed by MTT assay. The expression of CD3 and CD25 antigens on T lymphocytes were detected by flow cytometry. The levels of sIL-2R in the supernatants were determined with ELISA. The results showed that both rhCD25MAb and CsA could inhibit the proliferation of T lymphocytes significantly in concentration-dependent manner and CsA was more efficient than rhCD25MAb. Both rhCD25MAb and CsA could also decrease the levels of sIL-2R in the supernatant and inhibit the expression of CD25 antigen on T lymphocytes. The level of sIL-2R and the expression of CD25 on T lymphocytes decreases more profoundly in rhCD25MAb group. It is concluded that rhCD25MAb shows strong immunosuppressive activity both before and after T cell activation, suggesting that this agent may be useful in not only prophylaxis but also the treatment of acute graft-versus-host disease.
