What is he best known for?
The fields of study he is best known for:
- Gene
- Immune system
- Cytokine
Robert L. Modlin focuses on Immunology, Cell biology, T cell, TLR2 and Microbiology.
His studies in Immunology integrate themes in fields like Interleukin 12 and In vivo.
His study in Cell biology is interdisciplinary in nature, drawing from both Innate immune system, CD86 and CD40.
His T cell study integrates concerns from other disciplines, such as Cytotoxic T cell, CD8, Antigen and Interferon gamma.
His work is dedicated to discovering how TLR2, Toll-like receptor are connected with Lipopeptide and Stimulation and other disciplines.
His Microbiology research includes themes of Macrophage and Intracellular.
His most cited work include:
- Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response (2850 citations)
- Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors. (1527 citations)
- Cutting Edge: Role of Toll-Like Receptor 1 in Mediating Immune Response to Microbial Lipoproteins (1171 citations)
What are the main themes of his work throughout his whole career to date?
Robert L. Modlin spends much of his time researching Immunology, Immune system, Microbiology, Cell biology and Innate immune system.
T cell, Mycobacterium leprae, Cytokine, Immunity and Antigen are the subjects of his Immunology studies.
His T cell research incorporates themes from Cytotoxic T cell and Molecular biology.
His Immune system research is multidisciplinary, relying on both Inflammation, Vitamin D and neurology, Peripheral blood mononuclear cell and Pathogenesis.
As a part of the same scientific family, Robert L. Modlin mostly works in the field of Microbiology, focusing on Mycobacterium tuberculosis and, on occasion, Virology.
Innate immune system is a primary field of his research addressed under Receptor.
He most often published in these fields:
- Immunology (49.39%)
- Immune system (32.73%)
- Microbiology (25.45%)
What were the highlights of his more recent work (between 2014-2021)?
- Microbiology (25.45%)
- Immune system (32.73%)
- Mycobacterium leprae (15.76%)
In recent papers he was focusing on the following fields of study:
The scientist’s investigation covers issues in Microbiology, Immune system, Mycobacterium leprae, Immunology and Innate immune system.
The various areas that Robert L. Modlin examines in his Microbiology study include Autophagy, Interferon and Macrophage.
His Immune system research includes elements of Tumor necrosis factor alpha, Pathogenesis and Cell biology.
His work carried out in the field of Cell biology brings together such families of science as Interleukin 12 and Cytokine.
His research on Immunology frequently connects to adjacent areas such as Infectious disease.
His study in the field of Pattern recognition receptor is also linked to topics like Signal, Interaction mode and Code.
Between 2014 and 2021, his most popular works were:
- STING activation of tumor endothelial cells initiates spontaneous and therapeutic antitumor immunity (194 citations)
- TH17 cells promote microbial killing and innate immune sensing of DNA via interleukin 26 (133 citations)
- Bee venom processes human skin lipids for presentation by CD1a (68 citations)
In his most recent research, the most cited papers focused on:
- Gene
- Immune system
- Cytokine
His primary areas of study are Microbiology, Immune system, Immunology, Innate immune system and Immunity.
His Microbiology research includes elements of Mycobacterium leprae and Macrophage.
His work in the fields of TLR2, Cathelicidin and Antigen presentation overlaps with other areas such as Bee Venoms.
His research investigates the link between TLR2 and topics such as Intracellular parasite that cross with problems in Mycobacterium tuberculosis.
As a part of the same scientific study, Robert L. Modlin usually deals with the Immunology, concentrating on Virology and frequently concerns with Attenuated vaccine.
His Innate immune system research is multidisciplinary, incorporating perspectives in Biological pathway and Interferon.
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