Heinz G. Remold focuses on Macrophage, Apoptosis, Molecular biology, Mycobacterium tuberculosis and Microbiology. His Macrophage research incorporates elements of Calcitonin, Endocrinology, Phagocytosis and Plasma membrane repair, Cell membrane. The Apoptosis study combines topics in areas such as Necrosis, Tumor necrosis factor alpha and Cell biology.
His Molecular biology study combines topics from a wide range of disciplines, such as In vitro, Macrophage migration inhibitory factor, Chemotaxis, Immunology and Binding site. His biological study spans a wide range of topics, including Virology, Antigen presentation, Immunity and Virulence. He works mostly in the field of Microbiology, limiting it down to topics relating to Intracellular and, in certain cases, Cytolysis and Caspase 3.
Heinz G. Remold mainly focuses on Molecular biology, Macrophage, Biochemistry, Immunology and Microbiology. His Molecular biology research incorporates themes from Macrophage migration inhibitory factor, Lymphokine, Antigen, Peripheral blood mononuclear cell and Sephadex. His Macrophage research includes elements of Apoptosis, Cell, Receptor and Cell biology.
Concanavalin A is closely connected to Guinea pig in his research, which is encompassed under the umbrella topic of Biochemistry. His Immunology research focuses on subjects like Chemotaxis, which are linked to Cell Migration Inhibition and In vitro. His work deals with themes such as Tumor necrosis factor alpha, Cytokine, Mycobacterium, Virology and Mycobacterium tuberculosis, which intersect with Microbiology.
The scientist’s investigation covers issues in Cell biology, Apoptosis, Necrosis, Macrophage and Microbiology. His work carried out in the field of Cell biology brings together such families of science as Inflammation, Secretion and T cell. His research ties Molecular biology and Apoptosis together.
His work carried out in the field of Macrophage brings together such families of science as Intracellular, Programmed cell death and Plasma membrane repair. His Microbiology research is multidisciplinary, relying on both Annexin A1, Virology, Virulence and Mycobacterium tuberculosis. His Mycobacterium tuberculosis research includes elements of Antigen presentation and Immunity.
His primary scientific interests are in Necrosis, Apoptosis, Macrophage, Cell biology and Immunity. Heinz G. Remold works mostly in the field of Necrosis, limiting it down to concerns involving Prostaglandin E and, occasionally, Lipoxin, Lipid signaling and Prostaglandin E synthase. Much of his study explores Macrophage relationship to Plasma membrane repair.
His study in Cell biology is interdisciplinary in nature, drawing from both Tumor necrosis factor alpha, T cell, Inflammation and Programmed cell death. Heinz G. Remold has included themes like Acquired immune system, Innate immune system and Tuberculosis in his Immunity study. His work on Microbiology expands to the thematically related Mycobacterium tuberculosis.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Virulent Mycobacterium tuberculosis Strains Evade Apoptosis of Infected Alveolar Macrophages
Joseph Keane;Heinz G. Remold;Hardy Kornfeld.
Journal of Immunology (2000)
Infection by Mycobacterium tuberculosis promotes human alveolar macrophage apoptosis.
J Keane;M K Balcewicz-Sablinska;H G Remold;G L Chupp.
Infection and Immunity (1997)
Pathogenic Mycobacterium tuberculosis evades apoptosis of host macrophages by release of TNF-R2, resulting in inactivation of TNF-alpha
Balcewicz-Sablinska Mk;Keane J;Kornfeld H;Remold Hg.
Journal of Immunology (1998)
Molecular cloning of a cDNA encoding a human macrophage migration inhibitory factor.
Weishui Y. Weiser;Patricia A. Temple;Joann S. Witek-Giannotti;Heinz G. Remold.
Proceedings of the National Academy of Sciences of the United States of America (1989)
Activation of human macrophages. Comparison of other cytokines with interferon-gamma.
C F Nathan;T J Prendergast;M E Wiebe;E R Stanley.
Journal of Experimental Medicine (1984)
Evasion of innate immunity by Mycobacterium tuberculosis : is death an exit strategy?
Samuel M. Behar;Maziar Divangahi;Maziar Divangahi;Heinz G. Remold.
Nature Reviews Microbiology (2010)
Apoptosis is an innate defense function of macrophages against Mycobacterium tuberculosis
Behar Sm;Martin Cj;Booty Mg;Nishimura T.
Mucosal Immunology (2011)
Lipid mediators in innate immunity against tuberculosis: opposing roles of PGE2 and LXA4 in the induction of macrophage death
Minjian Chen;Maziar Divangahi;Huixian Gan;Daniel S.J. Shin.
Journal of Experimental Medicine (2008)
Mycobacterium tuberculosis evades macrophage defenses by inhibiting plasma membrane repair
Maziar Divangahi;Minjian Chen;Huixian Gan;Danielle Desjardins.
Nature Immunology (2009)
Macrophage Apoptosis in Response to High Intracellular Burden of Mycobacterium tuberculosis Is Mediated by a Novel Caspase-Independent Pathway
Jinhee Lee;Heinz G. Remold;Michael H. Ieong;Hardy Kornfeld.
Journal of Immunology (2006)
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below:
Harvard University
University of Massachusetts Medical School
University of Massachusetts Medical School
Tufts University
Colorado State University
National Institutes of Health
Harvard University
Tsinghua University
Medical University of Vienna
Tufts Medical Center
Sony (Japan)
Indian Institute of Technology Roorkee
RWTH Aachen University
Soochow University
Ulsan National Institute of Science and Technology
Alfred Wegener Institute for Polar and Marine Research
Fujian Agriculture and Forestry University
University of Maryland Center For Environmental Sciences
Boston Children's Hospital
Walter and Eliza Hall Institute of Medical Research
Ruhr University Bochum
University of Virginia
Southern Illinois University School of Medicine
University of Oxford
University of Melbourne
Stanford University