Inhibition of cell proliferation with an HLA-A-specific monoclonal antibody
| Autor: | David A. Scheinberg, K. A. Class, J. G. Minniti, M. K. Bull, Soo Young Yang |
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| Rok vydání: | 1991 |
| Předmět: |
medicine.drug_class
Immunoprecipitation Immunology Monoclonal antibody Biochemistry Peripheral blood mononuclear cell Immunoglobulin Fab Fragments Mice Genetics medicine Animals Humans Immunology and Allergy Cytotoxicity Mice Inbred BALB C HLA-A Antigens biology Cell growth Cell Cycle Antibodies Monoclonal RNA DNA General Medicine Cell cycle Molecular biology Immunoglobulin G Leukocytes Mononuclear biology.protein Antibody Cell Division |
| Zdroj: | Tissue Antigens. 38:213-223 |
| ISSN: | 1399-0039 0001-2815 |
| DOI: | 10.1111/j.1399-0039.1991.tb01900.x |
| Popis: | A new mouse IgG2A monoclonal antibody--JD 12--is described, which was selected for its ability to inhibit peripheral blood mononuclear cell (PBMC) proliferation. Serologic, immunoprecipitation and immunoelectrophoretic studies showed JD12 to be monomorphically reactive with HLA-A molecules with an affinity of 10(9) M-1. JD12 was capable of inhibiting growth in resting or stimulated PBMC with an ID50 of 300 ng/ml in a time-dependent and dose-dependent manner without cytotoxicity. IgG, F(ab)2 and F(ab) were active. Growth stimulation by phorbol ester was not inhibited, suggesting that JD12 action occurred prior to protein kinase C activation. DNA and RNA synthesis were both slowed with a resulting G0/G1 block. Analysis of separated PBMC components showed that adherent cells displayed increased activity (clumping and RNA synthesis) upon JD12 binding. In addition, the inhibitory activity of JD12 could be transferred to new cultures by cell-free, IgG-free supernatant from JD12-treated PBMC, suggesting that the antiproliferative effects could be mediated, at least in part, in an indirect manner through an inhibitory factor. Therefore, potent, noncytotoxic inhibition of cell proliferation, DNA and RNA synthesis via MHC molecules can be mediated specifically through effects initiated by binding to HLA-A molecules alone. |
| Databáze: | OpenAIRE |
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