The Experts below are selected from a list of 201 Experts worldwide ranked by ideXlab platform
Suzanne Ostrand-rosenberg - One of the best experts on this subject based on the ideXlab platform.
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High-mobility group box protein 1 promotes the survival of myeloid-derived Suppressor Cells by inducing autophagy.
Journal of Leukocyte Biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived Suppressor Cells are immune-suppressive Cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived Suppressor Cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule high-mobility group box protein 1 drives myeloid-derived Suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As high-mobility group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if high-mobility group box protein 1 regulates myeloid-derived Suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived Suppressor Cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived Suppressor Cells. Inhibition of high-mobility group box protein 1 similarly increased the level of apoptotic myeloid-derived Suppressor Cells and reduced myeloid-derived Suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived Suppressor Cells, high-mobility group box protein 1 sustains myeloid-derived Suppressor cell viability. Circulating myeloid-derived Suppressor Cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived Suppressor Cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived Suppressor Cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, high-mobility group box protein 1 contributes to tumor progression by increasing myeloid-derived Suppressor cell viability by driving them into a proautophagic state.
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High‐mobility group box protein 1 promotes the survival of myeloid‐derived Suppressor Cells by inducing autophagy
Journal of leukocyte biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived Suppressor Cells are immune-suppressive Cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived Suppressor Cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule high-mobility group box protein 1 drives myeloid-derived Suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As high-mobility group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if high-mobility group box protein 1 regulates myeloid-derived Suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived Suppressor Cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived Suppressor Cells. Inhibition of high-mobility group box protein 1 similarly increased the level of apoptotic myeloid-derived Suppressor Cells and reduced myeloid-derived Suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived Suppressor Cells, high-mobility group box protein 1 sustains myeloid-derived Suppressor cell viability. Circulating myeloid-derived Suppressor Cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived Suppressor Cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived Suppressor Cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, high-mobility group box protein 1 contributes to tumor progression by increasing myeloid-derived Suppressor cell viability by driving them into a proautophagic state.
Katherine H. Parker - One of the best experts on this subject based on the ideXlab platform.
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High-mobility group box protein 1 promotes the survival of myeloid-derived Suppressor Cells by inducing autophagy.
Journal of Leukocyte Biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived Suppressor Cells are immune-suppressive Cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived Suppressor Cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule high-mobility group box protein 1 drives myeloid-derived Suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As high-mobility group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if high-mobility group box protein 1 regulates myeloid-derived Suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived Suppressor Cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived Suppressor Cells. Inhibition of high-mobility group box protein 1 similarly increased the level of apoptotic myeloid-derived Suppressor Cells and reduced myeloid-derived Suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived Suppressor Cells, high-mobility group box protein 1 sustains myeloid-derived Suppressor cell viability. Circulating myeloid-derived Suppressor Cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived Suppressor Cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived Suppressor Cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, high-mobility group box protein 1 contributes to tumor progression by increasing myeloid-derived Suppressor cell viability by driving them into a proautophagic state.
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High‐mobility group box protein 1 promotes the survival of myeloid‐derived Suppressor Cells by inducing autophagy
Journal of leukocyte biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived Suppressor Cells are immune-suppressive Cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived Suppressor Cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule high-mobility group box protein 1 drives myeloid-derived Suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As high-mobility group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if high-mobility group box protein 1 regulates myeloid-derived Suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived Suppressor Cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived Suppressor Cells. Inhibition of high-mobility group box protein 1 similarly increased the level of apoptotic myeloid-derived Suppressor Cells and reduced myeloid-derived Suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived Suppressor Cells, high-mobility group box protein 1 sustains myeloid-derived Suppressor cell viability. Circulating myeloid-derived Suppressor Cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived Suppressor Cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived Suppressor Cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, high-mobility group box protein 1 contributes to tumor progression by increasing myeloid-derived Suppressor cell viability by driving them into a proautophagic state.
Dmitry I. Gabrilovich - One of the best experts on this subject based on the ideXlab platform.
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Biology of Myeloid-Derived Suppressor Cells
Oncoimmunology, 2017Co-Authors: Kevin Alicea-torres, Dmitry I. GabrilovichAbstract:The accumulation of highly immunosuppressive myeloid Cells known as myeloid-derived Suppressor Cells (MDSCs) is one of the immunological hallmarks of cancer. MDSCs are a heterogeneous population of bone marrow-derived immature myeloid Cells that accumulate in the blood, peripheral lymphoid organs, and tumor tissues, which correlates with a poor clinical outcome in cancer patients. The main feature of MDSCs is their ability to suppress antitumor responses leading to tumor progression. Thus, MDSCs represent an attractive therapeutic target to enhance antitumor responses in cancer.
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Myeloid-Derived Suppressor Cells
Cancer immunology research, 2017Co-Authors: Dmitry I. GabrilovichAbstract:Myeloid Cells developed evolutionarily as a major mechanism to protect the host. They evolved as a critical barrier against infections and are important contributors to tissue remodeling. However, in cancer, myeloid Cells are largely converted to serve a new master—tumor Cells. This process is epitomized by myeloid-derived Suppressor Cells (MDSC). These Cells are closely related to neutrophils and monocytes. MDSCs are not present in the steady state of healthy individuals and appear in cancer and in pathologic conditions associated with chronic inflammation or stress. These Cells have emerged as an important contributor to tumor progression. Ample evidence supports a key role for MDSCs in immune suppression in cancer, as well as their prominent role in tumor angiogenesis, drug resistance, and promotion of tumor metastases. MDSCs have a fascinating biology and are implicated in limiting the effects of cancer immunotherapy. Therefore, targeting these Cells may represent an attractive therapeutic opportunity. Cancer Immunol Res; 5(1); 3–8. ©2016 AACR .
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Transcriptional regulation of myeloid-derived Suppressor Cells
Journal of Leukocyte Biology, 2015Co-Authors: Thomas Condamine, Jerome Mastio, Dmitry I. GabrilovichAbstract:Abstract Myeloid-derived Suppressor Cells are a heterogeneous group of pathologically activated immature Cells that play a major role in the negative regulation of the immune response in cancer, autoimmunity, many chronic infections, and inflammatory conditions, as well as in the regulation of tumor angiogenesis, tumor cell invasion, and metastases. Accumulation of myeloid-derived Suppressor Cells is governed by a network of transcriptional regulators that could be combined into 2 partially overlapping groups: factors promoting myelopoiesis and preventing differentiation of mature myeloid Cells and factors promoting pathologic activation of myeloid-derived Suppressor Cells. In this review, we discuss the specific nature of these factors and their impact on myeloid-derived Suppressor cell development.
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ROR1C Regulates Differentiation of Myeloid-Derived Suppressor Cells
Cancer Cell, 2015Co-Authors: Dmitry I. Gabrilovich, Yulia NefedovaAbstract:Myeloid-derived Suppressor Cells (MDSCs) play a major role in cancer. MDSC expansion is closely associated with tumor progression, but molecular mechanisms of this expansion remain poorly understood. In this issue of Cancer Cell, Strauss and colleagues describe the roles of the nuclear receptor ROR1C in the regulation of MDSC differentiation and expansion.
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History of myeloid-derived Suppressor Cells.
Nature Reviews Cancer, 2013Co-Authors: James E. Talmadge, Dmitry I. GabrilovichAbstract:Tumour-induced granulocytic hyperplasia is associated with tumour vasculogenesis and escape from immunity via T cell suppression. Initially, these myeloid Cells were identified as granulocytes or monocytes; however, recent studies have revealed that this hyperplasia is associated with populations of multipotent progenitor Cells that have been identified as myeloid-derived Suppressor Cells (MDSCs). The study of MDSCs has provided a wealth of information regarding tumour pathobiology, has extended our understanding of neoplastic progression and has modified our approaches to immune adjuvant therapy. In this Timeline article, we discuss the history of MDSCs, their influence on tumour progression and metastasis, and the crosstalk between tumour Cells, MDSCs and the host macroenvironment.
Lucas A. Horn - One of the best experts on this subject based on the ideXlab platform.
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High-mobility group box protein 1 promotes the survival of myeloid-derived Suppressor Cells by inducing autophagy.
Journal of Leukocyte Biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived Suppressor Cells are immune-suppressive Cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived Suppressor Cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule high-mobility group box protein 1 drives myeloid-derived Suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As high-mobility group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if high-mobility group box protein 1 regulates myeloid-derived Suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived Suppressor Cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived Suppressor Cells. Inhibition of high-mobility group box protein 1 similarly increased the level of apoptotic myeloid-derived Suppressor Cells and reduced myeloid-derived Suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived Suppressor Cells, high-mobility group box protein 1 sustains myeloid-derived Suppressor cell viability. Circulating myeloid-derived Suppressor Cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived Suppressor Cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived Suppressor Cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, high-mobility group box protein 1 contributes to tumor progression by increasing myeloid-derived Suppressor cell viability by driving them into a proautophagic state.
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High‐mobility group box protein 1 promotes the survival of myeloid‐derived Suppressor Cells by inducing autophagy
Journal of leukocyte biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived Suppressor Cells are immune-suppressive Cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived Suppressor Cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule high-mobility group box protein 1 drives myeloid-derived Suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As high-mobility group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if high-mobility group box protein 1 regulates myeloid-derived Suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived Suppressor Cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived Suppressor Cells. Inhibition of high-mobility group box protein 1 similarly increased the level of apoptotic myeloid-derived Suppressor Cells and reduced myeloid-derived Suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived Suppressor Cells, high-mobility group box protein 1 sustains myeloid-derived Suppressor cell viability. Circulating myeloid-derived Suppressor Cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived Suppressor Cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived Suppressor Cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, high-mobility group box protein 1 contributes to tumor progression by increasing myeloid-derived Suppressor cell viability by driving them into a proautophagic state.
Srinivas Nagaraj - One of the best experts on this subject based on the ideXlab platform.
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25 Role of Myeloid Derived Suppressor Cells in Asthma
World Allergy Organization Journal, 2012Co-Authors: Allison Nelson, Jim Parkerson, Richard F. Lockey, Subhra Mohapatra, Shyam S. Mohapatra, Srinivas NagarajAbstract:Background We know that a heterogeneous group of myeloid Cells termed myeloid derived Suppressor Cells (MDSC) accumulate in almost all pathological conditions, which elicit an inflammatory signal. The exact role played by these Cells in asthma is not known. In this study we investigated the function and role of these Cells in asthma.
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Myeloid-derived Suppressor Cells in human cancer.
Cancer Journal, 2010Co-Authors: Srinivas Nagaraj, Dmitry I. GabrilovichAbstract:Myeloid-derived Suppressor Cells are one of the major factors responsible for immune suppression in cancer. They also contribute to limited efficacy of current vaccination strategies. Here, we give an overview of the myeloid-derived Suppressor Cells field focusing primarily on the studies in cancer patients and current and future therapeutic options targeting these Cells.
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myeloid derived Suppressor Cells as regulators of the immune system
Nature Reviews Immunology, 2009Co-Authors: Dmitry I. Gabrilovich, Srinivas NagarajAbstract:Myeloid-derived Suppressor Cells (MDSCs) are a heterogeneous population of Cells that expands during cancer, inflammation and infection. Here, the authors discuss the mechanisms of MDSC expansion and suppression of T-cell function in vivo, and describe how these Cells might be targeted for therapeutic purposes.
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Tumor Escape Mechanism Governed by Myeloid-Derived Suppressor Cells
Cancer Research, 2008Co-Authors: Srinivas Nagaraj, Dmitry I. GabrilovichAbstract:T-cell nonresponsiveness is a critical factor in immune escape and myeloid-derived Suppressor Cells play a major role in organizing this phenomenon. Recent findings indicate that myeloid-derived Suppressor Cells can induce antigen-specific CD8+ T-cell tolerance through a posttranslation mechanism which involves modification (nitration) of CD8 and the T-cell receptor itself on the T-cell surface. Elucidation of this mechanism of T-cell tolerance offers new opportunities for therapeutic corrections of immune escape in cancer. [Cancer Res 2008;68(8):2561–63]
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Myeloid-Derived Suppressor Cells
Advances in Experimental Medicine and Biology, 2007Co-Authors: Srinivas Nagaraj, Dmitry I. GabrilovichAbstract:The development of tumor-specific T cell tolerance is largely responsible for tumor escape. Accumulation of myeloid-derived Suppressor Cells (MDSCs) in animal tumor models as well as in cancer patients is involved in tumor-associated T cell tolerance. In recent years, it has become increasingly evident that MDSCs bring about antigen-specific T cell tolerance by various mechanisms, which is the focus of this chapter.