Her primary areas of study are Immunology, Cytokine, Interleukin 13, Immune system and Asthma. Her study in Immunology concentrates on Interleukin, Antigen, Allergy, Allergic response and Immunoglobulin E. Her Cytokine study integrates concerns from other disciplines, such as Peripheral blood mononuclear cell, Regulation of gene expression, Case-control study and Incubation.
Marsha Wills-Karp has included themes like Interleukin 23, Interleukin 17, Complement C5a and Complement receptor in her Interleukin 13 study. Her work on Inactivated vaccine as part of her general Immune system study is frequently connected to Viral pneumonia, thereby bridging the divide between different branches of science. Her study in Asthma is interdisciplinary in nature, drawing from both Mediator and Tralokinumab.
Marsha Wills-Karp focuses on Immunology, Asthma, Immune system, Cytokine and Interleukin 13. Her Immunology study frequently intersects with other fields, such as Lung. The various areas that Marsha Wills-Karp examines in her Asthma study include Respiratory disease, Disease and Genetics, Gene.
Marsha Wills-Karp has researched Interleukin 13 in several fields, including STAT6, House dust mite, Receptor and Signal transduction, Cell biology. Her Inflammation research is multidisciplinary, incorporating elements of Eosinophilia and Pathogenesis. Her biological study spans a wide range of topics, including Allergic response and Interleukin.
Marsha Wills-Karp mostly deals with Immunology, Inflammation, Immune system, Asthma and Interleukin 13. Her Immunology study combines topics from a wide range of disciplines, such as Signal transduction, Disease and Lung. Marsha Wills-Karp interconnects Endocrinology, Cytokine and Lymphocyte in the investigation of issues within Inflammation.
Her Immune system research is multidisciplinary, relying on both Microbiome, Expression quantitative trait loci, Tropomyosin and Pharmacology. Her Asthma research integrates issues from Leukocytosis and Bioinformatics. Her Interleukin 13 research includes themes of STAT6, Blockade and Cell biology.
The scientist’s investigation covers issues in Immunology, Interleukin 13, Signal transduction, Immune system and Inflammation. Her Immunology study integrates concerns from other disciplines, such as Blockade and Interleukin 12. Her work in Interleukin 12 covers topics such as Cytokine which are related to areas like Asthma.
While the research belongs to areas of Interleukin 13, she spends her time largely on the problem of STAT6, intersecting her research to questions surrounding Gene expression, Cell biology, Cell culture and Interleukin 17. Her work deals with themes such as Interleukin, Regulation of gene expression, Cancer research and Keratin, which intersect with Signal transduction. Her study in Immune system is interdisciplinary in nature, drawing from both Microbiome, Human microbiome, Gut flora and Entamoeba histolytica.
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.
Interleukin-13: Central Mediator of Allergic Asthma
M. Wills-Karp;J. Luyimbazi;X. Xu;B. Schofield.
Science (1998)
IMMUNOLOGIC BASIS OF ANTIGEN-INDUCED AIRWAY HYPERRESPONSIVENESS
Marsha Wills-Karp.
Annual Review of Immunology (1999)
The germless theory of allergic disease: revisiting the hygiene hypothesis
Marsha Wills-Karp;Joanna Santeliz;Christopher L. Karp.
Nature Reviews Immunology (2001)
Interleukin-13 in asthma pathogenesis
Marsha Wills-Karp.
Immunological Reviews (2004)
Allergenicity resulting from functional mimicry of a Toll-like receptor complex protein
Aurelien Trompette;Senad Divanovic;Alberto Visintin;Carine Blanchard.
Nature (2009)
Interleukin 12 inhibits antigen-induced airway hyperresponsiveness, inflammation, and Th2 cytokine expression in mice.
Stephen H. Gavett;Daniel J. O’Hearn;Xiumin Li;Shau Ku Huang.
Journal of Experimental Medicine (1995)
Depletion of murine CD4+ T lymphocytes prevents antigen-induced airway hyperreactivity and pulmonary eosinophilia.
S. H. Gavett;Xiaoling Chen;F. Finkelman;M. Wills-Karp.
American Journal of Respiratory Cell and Molecular Biology (1994)
Signal Transducer and Activator of Transcription Factor 6 (Stat6)-deficient Mice Are Protected from Antigen-induced Airway Hyperresponsiveness and Mucus Production
Douglas Kuperman;Brian Schofield;Marsha Wills-Karp;Michael J. Grusby.
Journal of Experimental Medicine (1998)
CD4+CD25+ T cells protect against experimentally induced asthma and alter pulmonary dendritic cell phenotype and function
Ian P. Lewkowich;Nancy S. Herman;Kathleen W. Schleifer;Matthew P. Dance.
Journal of Experimental Medicine (2005)
Identification of complement factor 5 as a susceptibility locus for experimental allergic asthma.
Christopher L. Karp;Andrew Grupe;Eric Schadt;Susan L. Ewart.
Nature Immunology (2000)
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:
University of Cincinnati
Bill & Melinda Gates Foundation
Cincinnati Children's Hospital Medical Center
University of Lübeck
Johns Hopkins University
Cincinnati Children's Hospital Medical Center
Johns Hopkins University
Cincinnati Children's Hospital Medical Center
University of Colorado Anschutz Medical Campus
Johns Hopkins University
University of Bologna
University of Michigan–Ann Arbor
University of Western Ontario
Carl von Ossietzky University of Oldenburg
Texas A&M University
National Institute of Standards and Technology
University College London
University of California, Davis
Research Institute of Molecular Pathology
Harvard University
ETH Zurich
Monash University
Harvard University
University of Minnesota
University of Lausanne
Heidelberg University