The Experts below are selected from a list of 36 Experts worldwide ranked by ideXlab platform
Salem Chouaib - One of the best experts on this subject based on the ideXlab platform.
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Hypoxia: a key player in Antitumor immune response. A Review in the Theme: Cellular Responses to Hypoxia
American Journal of Physiology - Cell Physiology, 2015Co-Authors: Muhammad Zaeem Noman, Meriem Hasmim, Yosra Messai, Stephane Terry, Claudine Kieda, Bassam Janji, Salem ChouaibAbstract:The tumor microenvironment is a complex system, playing an important role in tumor development and progression. Besides Cellular stromal components, extraCellular matrix fibers, cytokines, and other metabolic mediators are also involved. In this review we outline the potential role of hypoxia, a major feature of most solid tumors, within the tumor microenvironment and how it contributes to immune resistance and immune suppression/tolerance and can be detrimental to Antitumor Effector Cell functions. We also outline how hypoxic stress influences immunosuppressive pathways involving macrophages, myeloid-derived suppressor Cells, T regulatory Cells, and immune checkpoints and how it may confer tumor resistance. Finally, we discuss how microenvironmental hypoxia poses both obstacles and opportunities for new therapeutic immune interventions.
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Hypoxia-induced autophagy: a new player in cancer immunotherapy?
Autophagy, 2012Co-Authors: Muhammad Zaeem Noman, Bassam Janji, Guy Berchem, Fathia Mami-chouaib, Salem ChouaibAbstract:A major challenge in formulating an effective immunotherapy is to overcome the mechanisms of tumor escape from immunosurveillance. We showed that hypoxia-induced autophagy impairs cytotoxic T-lymphocyte (CTL)-mediated tumor Cell lysis by regulating phospho-STAT3 in target Cells. Autophagy inhibition in hypoxic Cells decreases phospho-STAT3 and restores CTL-mediated tumor Cell killing by a mechanism involving the ubiquitin proteasome system and SQSTM1/p62. Simultaneously boosting the CTL-response, using a TRP-peptide vaccination strategy, and targeting autophagy in hypoxic tumors, improves the efficacy of cancer vaccines and promotes tumor regression in vivo. Overall, in addition to its immunosuppressive effect, the hypoxic microenvironment also contributes to immunoresistance and can be detrimental to Antitumor Effector Cell functions.
Muhammad Zaeem Noman - One of the best experts on this subject based on the ideXlab platform.
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Hypoxia: a key player in Antitumor immune response. A Review in the Theme: Cellular Responses to Hypoxia
American Journal of Physiology - Cell Physiology, 2015Co-Authors: Muhammad Zaeem Noman, Meriem Hasmim, Yosra Messai, Stephane Terry, Claudine Kieda, Bassam Janji, Salem ChouaibAbstract:The tumor microenvironment is a complex system, playing an important role in tumor development and progression. Besides Cellular stromal components, extraCellular matrix fibers, cytokines, and other metabolic mediators are also involved. In this review we outline the potential role of hypoxia, a major feature of most solid tumors, within the tumor microenvironment and how it contributes to immune resistance and immune suppression/tolerance and can be detrimental to Antitumor Effector Cell functions. We also outline how hypoxic stress influences immunosuppressive pathways involving macrophages, myeloid-derived suppressor Cells, T regulatory Cells, and immune checkpoints and how it may confer tumor resistance. Finally, we discuss how microenvironmental hypoxia poses both obstacles and opportunities for new therapeutic immune interventions.
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Hypoxia-induced autophagy: a new player in cancer immunotherapy?
Autophagy, 2012Co-Authors: Muhammad Zaeem Noman, Bassam Janji, Guy Berchem, Fathia Mami-chouaib, Salem ChouaibAbstract:A major challenge in formulating an effective immunotherapy is to overcome the mechanisms of tumor escape from immunosurveillance. We showed that hypoxia-induced autophagy impairs cytotoxic T-lymphocyte (CTL)-mediated tumor Cell lysis by regulating phospho-STAT3 in target Cells. Autophagy inhibition in hypoxic Cells decreases phospho-STAT3 and restores CTL-mediated tumor Cell killing by a mechanism involving the ubiquitin proteasome system and SQSTM1/p62. Simultaneously boosting the CTL-response, using a TRP-peptide vaccination strategy, and targeting autophagy in hypoxic tumors, improves the efficacy of cancer vaccines and promotes tumor regression in vivo. Overall, in addition to its immunosuppressive effect, the hypoxic microenvironment also contributes to immunoresistance and can be detrimental to Antitumor Effector Cell functions.
James E. Talmadge - One of the best experts on this subject based on the ideXlab platform.
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Effect of tumor burden and route of administration on the immunotherapeutic properties of polyinosinic-polycytidylic acid stabilized with poly-L-lysine in carboxymethyl Cellulose [Poly(I,C)-LC].
International journal of immunopharmacology, 1992Co-Authors: Paul L. Black, Diethelm Hartmann, Robin Pennington, Hamblin Phillips, Mark Schneider, Henry Tribble, James E. TalmadgeAbstract:Abstract We examined the immunomodulatory and therapeutic activities of poly(I,C-LC. Mice received a subcutaneous (s.c.) injection of sufficient numbers of MBL-2 lymphoma Cells to produce in 1 week either a high or low tumor burden. A week after tumor Cell injection, poly(I,C)-LC treatment was initieated; the agent was administered intraperitoneally (i.p.) at 5 mg/kg twice a week or at 2.5 or 0.5 mg/kg every day or as an intravenous (i.v.) injection at 0.5, 0.05, or 0.005 mg/kg three times a week. Poly(I,C)-LC treatment significantly increased Antitumor Effector Cell functions in a variey of organs (including spleen, lungs, and peritoneum), as shown by increased killing of MBL-2 Cells in vitro and increased tumor Cell killing by natural killer Cells and macrophages. Furthermore, prolongation of survival correlated with peritoneal macrophage tumoricidal activity when poly(I,C)-LC was given i.p. and with pulmonary Effector Cell function (including natural killer, cytolytic T-lymphocyte and macrophage tumoricidal activity) when the agent was administered i.v.
Bassam Janji - One of the best experts on this subject based on the ideXlab platform.
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Hypoxia: a key player in Antitumor immune response. A Review in the Theme: Cellular Responses to Hypoxia
American Journal of Physiology - Cell Physiology, 2015Co-Authors: Muhammad Zaeem Noman, Meriem Hasmim, Yosra Messai, Stephane Terry, Claudine Kieda, Bassam Janji, Salem ChouaibAbstract:The tumor microenvironment is a complex system, playing an important role in tumor development and progression. Besides Cellular stromal components, extraCellular matrix fibers, cytokines, and other metabolic mediators are also involved. In this review we outline the potential role of hypoxia, a major feature of most solid tumors, within the tumor microenvironment and how it contributes to immune resistance and immune suppression/tolerance and can be detrimental to Antitumor Effector Cell functions. We also outline how hypoxic stress influences immunosuppressive pathways involving macrophages, myeloid-derived suppressor Cells, T regulatory Cells, and immune checkpoints and how it may confer tumor resistance. Finally, we discuss how microenvironmental hypoxia poses both obstacles and opportunities for new therapeutic immune interventions.
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Hypoxia-induced autophagy: a new player in cancer immunotherapy?
Autophagy, 2012Co-Authors: Muhammad Zaeem Noman, Bassam Janji, Guy Berchem, Fathia Mami-chouaib, Salem ChouaibAbstract:A major challenge in formulating an effective immunotherapy is to overcome the mechanisms of tumor escape from immunosurveillance. We showed that hypoxia-induced autophagy impairs cytotoxic T-lymphocyte (CTL)-mediated tumor Cell lysis by regulating phospho-STAT3 in target Cells. Autophagy inhibition in hypoxic Cells decreases phospho-STAT3 and restores CTL-mediated tumor Cell killing by a mechanism involving the ubiquitin proteasome system and SQSTM1/p62. Simultaneously boosting the CTL-response, using a TRP-peptide vaccination strategy, and targeting autophagy in hypoxic tumors, improves the efficacy of cancer vaccines and promotes tumor regression in vivo. Overall, in addition to its immunosuppressive effect, the hypoxic microenvironment also contributes to immunoresistance and can be detrimental to Antitumor Effector Cell functions.
Peeyush K. Lala - One of the best experts on this subject based on the ideXlab platform.
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Role of nitric oxide in IL-2 therapy-induced capillary leak syndrome.
Cancer metastasis reviews, 1998Co-Authors: Amila Orucevic, Peeyush K. LalaAbstract:Nitric oxide (NO) is a potent short-lived and short range bioactive molecule, which plays a key role in physiological and pathological processes including inflammation and cancer. Detrimental effects of excessive NO production during septic shock have been well recognized. We tested the hypothesis that 'capillary leak syndrome' following systemic interleukin-2 (IL-2) therapy resulted from a cascade of events leading to the induction of NO which, directly or indirectly, injured capillaries and caused fluid leakage. Our results provided the first direct evidence that the induction of active NO synthase (NOS) leading to the overproduction of NO is instrumental in IL-2-induced capillary leakage in mice and that successful blocking of this overproduction with chronic oral administration of NOS inhibitors can mitigate this leakage without interfering with the beneficial Antitumor effects of IL-2 therapy. NO blocking agents can, in fact, improve IL-2-induced Antitumor Effector Cell activation, as well as tumor regression. In our studies, NO blocking agents alone reduced the growth and metastasis of a murine mammary carcinoma, at least in part, by mitigating the invasion and angiogenesis-stimulating role of tumor-derived NO. Thus, NOS inhibitors may be useful in treating certain tumors and serve as valuable adjuncts to systemic IL-2 based immunotherapy of cancer and infectious diseases.