Cytolytic cells induce HMGB1 release from melanoma cell lines
| العنوان: | Cytolytic cells induce HMGB1 release from melanoma cell lines |
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| المؤلفون: | Robbie B. Mailliard, Jie Han, Herbert J. Zeh, Donna B. Stolz, Norimasa Ito, Pawel Kalinski, Richard A. DeMarco, Hannah Rabinowich, Michael T. Lotze |
| المصدر: | Journal of Leukocyte Biology. 81:75-83 |
| بيانات النشر: | Oxford University Press (OUP), 2006. |
| سنة النشر: | 2006 |
| مصطلحات موضوعية: | T-Lymphocytes, medicine.medical_treatment, Immunology, Active Transport, Cell Nucleus, chemical and pharmacologic phenomena, Biology, Granzymes, Amino Acid Chloromethyl Ketones, TNF-Related Apoptosis-Inducing Ligand, Immune system, Cell Line, Tumor, medicine, Humans, Immunology and Allergy, Macrophage, HMGB1 Protein, Killer Cells, Lymphokine-Activated, Melanoma, Cells, Cultured, Cell Nucleus, Tumor microenvironment, Cell Death, Cell Biology, Immunotherapy, Cytotoxicity Tests, Immunologic, Flow Cytometry, Cell biology, Granzyme B, Cytolysis, Granzyme, Cell culture, biology.protein |
| الوصف: | High mobility group box 1 (HMGB1) is one of the recently defined damage-associated molecular pattern molecules, passively released from necrotic cells and secreted by activated macrophage/monocytes. Whether cytolytic cells induce HMGB1 release from tumor cells is not known. We developed a highly sensitive method for detecting intracellular HMGB1 in tumor cells, allowing analysis of the type of cell death and in particular, necrosis. We induced melanoma cell death with cytolytic lymphokine-activated killing (LAK) cells, tumor-specific cytolytic T lymphocytes, TRAIL, or granzyme B delivery and assessed intracellular HMGB1 retention or release to investigate the mechanism of HMGB1 release by cytolytic cells. HMGB1 release from melanoma cells (451Lu, WM9) was detected within 4 h and 24 h following incubation with IL-2-activated PBMC (LAK activity). HLA-A2 and MART1 or gp100-specific cytolytic T lymphocytes induced HMGB1 release from HLA-A2-positive and MART1-positive melanoma cells (FEM X) or T2 cell-loaded, gp100-specific peptides. TRAIL treatment, however, induced HMGB1 release, and it is interesting that this extrinsic pathway-mediated cell death was blocked with the pancaspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone. Conversely, granzyme B delivery did not induce HMGB1 release. HMGB1, along with other intracellular factors released from tumor cells induced by cytolysis, may be important components of the disordered tumor microenvironment. This has important implications for the immunotherapy of patients with cancer. Specifically, HMGB1 may promote healing or immune reactivity, depending on the nature of the local inflammatory response and the presence (or absence) of immune effectors. |
| تدمد: | 1938-3673 0741-5400 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3f82c1ff130194209bdd05a507fb7698Test https://doi.org/10.1189/jlb.0306169Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....3f82c1ff130194209bdd05a507fb7698 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 19383673 07415400 |
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