Regulation of the expression on mouse T lymphocytes of the epitope identified by monoclonal antibody 3A35 |
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| Authors: | R le Corre Y le Garrec D Gerlier G Corradin L Toujas |
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| Affiliation: | 1. Laboratoire d''Immunologie du Centre Régional de Lutte contre le Cancer, Rennes, France;2. Laboratoire d''Immunothérapie Expérimentale, Institut Pasteur, Paris, France;3. Unité INSERM 218, Centre Léon Bérard, Lyon, France;4. Institut de Biochimie, Epalinges, Lausanne, Switzerland;1. Department of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China;2. Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangzhou, Guangdong 510080, China;3. Biomedical Pioneering Innovation Center (BIOPIC), Peking-Tsinghua Center for Life Sciences, School of Life Sciences, Peking University, Beijing, China;4. Beijing Advanced Innovation Center for Genomics, Peking University, Beijing, China;5. Department of Cell Biology, National Health Commission Key Laboratory of Antibody Techniques, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, Jiangsu 211166, China;6. Department of Scientific Research Section, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China;7. Institute of Pathology and Southwest Cancer Centre, Key Laboratory of Tumor Immunopathology of the Ministry of Education of China, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing 400038, China;8. Yu-Yue Pathology Scientific Research Center and Jinfeng Laboratory, Chongqing 400039, China;1. Institute for Cancer Genetics, and Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians & Surgeons, Columbia University, New York, NY, USA;2. Department of Pathology and Cell Biology, Vagelos College of Physicians & Surgeons, Columbia University, New York, NY, USA;1. Department of Medical Oncology, Oncode Institute, Leiden University Medical Center, Leiden 2333ZA, the Netherlands;2. Department of Pathology, Leiden University Medical Center, Leiden 2333ZA, the Netherlands;3. Department of Pathology, University of Chicago, Chicago, IL 60637, USA;4. Pritzker School of Molecular Engineering, Chicago, IL 60637, USA;5. Genmab, Utrecht 3584CT, the Netherlands |
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| Abstract: | Monoclonal antibody 3A35 (MA 3A35) has previously been shown to be an activation marker of macrophages and T lymphocytes. It immunoprecipitated from macrophages a 200-kDa molecule belonging to the T200 family and from T cells a 85-kDa antigen. In the present work, the factors controlling the expression of the epitope identified by MA 3A35 on polyclonal activated T cells and T-cell clones, as well as the ability of 3A35 alone or together with complement to interfere with T-cell functions, were investigated. Corticoresistant thymocytes unreactive with MA 3A35 became fully reactive after 2 days of in vitro stimulation by PMA and IL-2 and the level of reactivity per cell declined to a low level thereafter. In helper and cytolytic T-cell clones, the expression of the epitope defined by MA 3A35 was also maximal soon after antigenic stimulation then declined. In helper-T-cell clones, the epitope remained detectable during the entire culture period, whereas in cytolytic clones its expression was markedly reduced at the end of the culture. The lineage of cytotoxic T lymphocytes (CTL) as studied in a bulk culture of spleen cells primed in vivo against a syngeneic tumor exhibited similar regulation by antigenic stimulation. The CTL precursors were resistant to lysis by MA 3A35 plus complement; after 3 days of culture with the stimulatory antigen, they became highly sensitive but their sensitivity then diminished and mature CTL were completely resistant. MA 3A35 plus complement also killed the activated T cells which responded to macrophage-presented antigens and were thought to be mainly Lyt-1+. Therefore, the epitope identified by MA 3A35 was expressed predominantly at an early stage of T-cell activation. At a late stage, it persisted almost exclusively on helper and Lyt-1+ cells. In addition, MA 3A35 plus complement lysed NK cells, AK cells, and their precursors present in normal spleen. In the absence of complement, MA 3A35 had no detectable effect on T-cell functions. |
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