What is he best known for?
The fields of study he is best known for:
- Immune system
- Internal medicine
- Gene
The scientist’s investigation covers issues in Immunology, Apoptosis, Inflammation, Cell biology and Macrophage.
David H. Dockrell studies Viral load which is a part of Immunology.
His Apoptosis study combines topics from a wide range of disciplines, such as Innate immune system, Phagocytosis, Microbiology and Downregulation and upregulation.
His work carried out in the field of Phagocytosis brings together such families of science as Antibody, Programmed cell death and Monocyte.
His Microbiology study combines topics in areas such as Pseudomonas aeruginosa and Immune system.
His research integrates issues of Lipopolysaccharide and Lung injury in his study of Inflammation.
His most cited work include:
- The Identification of Markers of Macrophage Differentiation in PMA-Stimulated THP-1 Cells and Monocyte-Derived Macrophages (691 citations)
- Macrophage-dependent Apoptosis of CD4+ T Lymphocytes from HIV-infected Individuals Is Mediated by FasL and Tumor Necrosis Factor (226 citations)
- Alveolar Macrophage Apoptosis Contributes to Pneumococcal Clearance in a Resolving Model of Pulmonary Infection (190 citations)
What are the main themes of his work throughout his whole career to date?
His primary areas of investigation include Immunology, Apoptosis, Microbiology, Macrophage and Inflammation.
He has included themes like COPD, Lung and Streptococcus pneumoniae in his Immunology study.
The study incorporates disciplines such as Cancer research, Pathogenesis and Cell biology in addition to Apoptosis.
His Cancer research research includes elements of Kinase and ErbB.
In his research on the topic of Microbiology, Pathogen is strongly related with Staphylococcus aureus.
His Inflammation research incorporates elements of Bronchoalveolar lavage and Lung injury.
He most often published in these fields:
- Immunology (57.29%)
- Apoptosis (27.08%)
- Microbiology (16.67%)
What were the highlights of his more recent work (between 2018-2021)?
- Immunology (57.29%)
- Macrophage (18.75%)
- Inflammation (19.27%)
In recent papers he was focusing on the following fields of study:
David H. Dockrell focuses on Immunology, Macrophage, Inflammation, Immune system and Cell biology.
His Immunology research is mostly focused on the topic Myeloid.
The study incorporates disciplines such as Intracellular parasite, Apoptosis, Microbiology, Defective metabolism and Motility in addition to Macrophage.
His work is dedicated to discovering how Inflammation, Bronchoalveolar lavage are connected with Haemophilus influenzae, Chemokine, TLR4 and Granulocyte and other disciplines.
His work in Immune system tackles topics such as Pathogen which are related to areas like Antimicrobial and Antibiotic resistance.
The Cell biology study combines topics in areas such as Histone, Epigenetics and Pneumolysin.
Between 2018 and 2021, his most popular works were:
- Genome-wide CRISPR screen identifies host dependency factors for influenza A virus infection (37 citations)
- Defective bacterial phagocytosis is associated with dysfunctional mitochondria in COPD macrophages. (27 citations)
- The clock gene Bmal1 inhibits macrophage motility, phagocytosis, and impairs defense against pneumonia. (16 citations)
In his most recent research, the most cited papers focused on:
- Immune system
- Internal medicine
- Gene
David H. Dockrell spends much of his time researching Macrophage, Immunology, Inflammation, Apoptosis and Bronchoalveolar lavage.
His research integrates issues of Genetically modified mouse, Nitric oxide, Tuberculosis and Microbiology in his study of Macrophage.
He studies Microglia, a branch of Immunology.
David H. Dockrell has researched Inflammation in several fields, including Oxidative stress, Mitochondrion, Mitochondrial ROS, Phagocytosis and Granulocyte.
His research in Apoptosis focuses on subjects like ErbB, which are connected to Lung injury.
His Bronchoalveolar lavage study combines topics from a wide range of disciplines, such as Chemokine, Immune system, TLR4 and COPD.
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