Inverse relationship in H-2-associated lysis between NK cells and rIL-2-activated killer cells: evidence from in vitro killing and metastatic experiments |
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| Authors: | A Toshitani K Taniguchi Y Kawano K Nomoto |
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| Institution: | 1. Department of Graduate and Scientific Research, Zhuhai Campus of Zunyi Medical University, Zhuhai 519041, China;2. Department of Otolaryngology, Shenzhen Key Laboratory of Otolaryngology, Shenzhen Institute of Otolaryngology, Shenzhen Longgang Otolaryngology Hospital, Shenzhen, 518172, China;3. Department of Gastroenterology, Beijing University of Chinese Medicine Shenzhen Hospital (Longgang), Shenzhen 518172, China;1. Laboratory of Genome Integrity, Center for Cancer Research, NCI, NIH, Bethesda, MD, USA;2. Faculty of Medicine, Research Division, National Autonomous University of Mexico, Mexico City, Mexico;3. Children’s Hospital of Mexico Federico Gomez, Mexico City, Mexico;4. Metaorganism Immunity Section, Laboratory of Host Immunity and Microbiome, NIAID, NIH, Bethesda, MD, USA;5. Department of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA;6. Pediatric Oncology Branch, National Cancer Institute, NIH, Bethesda, MD, USA;7. Université de Nantes, CNRS, Inserm, CRCINA, Nantes, France;8. LabEx IGO “Immunotherapy, Graft, Oncology,” Nantes, France;9. Laboratory of Viral Diseases, NIAID, NIH, Bethesda, MD, USA;10. Genome Modification Core, Frederick National Laboratory for Cancer Research, Frederick, MD, USA;11. Mouse Modeling Core, Frederick National Laboratory for Cancer Research, Frederick, MD, USA;12. Oral Immunity and Infection Section, NIDCR, NIH, Bethesda, MD, USA;13. Shenzhen Typhoon HealthCare, Shenzhen, Guangdong, China;14. Laboratory of Immune System Biology, NIAID, NIH, Bethesda, MD, USA;15. Mucosal Immunology Section, NIDCR, NIH, Bethesda, MD, USA;16. Department of Immunology, Mayo Clinic, Rochester, MN, USA;1. School of Basic Medical Sciences, Fudan University, Shanghai 200433, China;2. Key Laboratory of Growth Regulation and Translational Research of Zhejiang Province, School of Life Sciences, Westlake University, Hangzhou 310024, Zhejiang, China;3. Center for Infectious Disease Research, Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou 310024, Zhejiang, China;4. Laboratory of Systems Immunology, Institute of Basic Medical Sciences, Westlake Institute for Advanced Study, Hangzhou 310024, Zhejiang, China;5. Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China;6. Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People’s Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai 200125, China;7. Laboratory of Neuroimmunology, Institute of Basic Medical Sciences, Westlake Institute for Advanced Study, Hangzhou 310024, Zhejiang, China |
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| Abstract: | We investigated the manner in which rIL-2 induced effectors in vitro (LAK cells), which, like NK cells, lyse targets nonspecifically and discriminate nonself, and how H-2 as the self-marker affects the LAK cell killing mechanism. NK cells showed an appreciably higher killing activity to B16 melanoma H-2- cells than to H-2+ cells. In contrast, LAK cells lysed more efficiently to H-2+ cells. The in vivo experiments showed that the NK cells prevented pulmonary metastasis of B16 H-2- cells in the normal syngeneic host, whereas the transferred LAK cells had a preferential inhibitory effect on the pulmonary metastasis of B16 H-2+ cells in the immunodeficient syngeneic hosts. Taken together, these results show that the H-2-encoded or H-2-associated molecules contribute to the triggering signal in the lysis by LAK cells, whereas the NK cells recognize the reduced self H-2 expression on the targets, thereby contributing to a trigger of the lysis. |
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