Debopam Ghosh
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Also affiliated: Indian Institute of Chemical Biology (2012); Institute of Post Graduate Medical Education and Research (2012); Stanford Medicine (2019–2022); Stanford University (2019–2022)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Debopam Ghosh's research investigates the intricate mechanisms of host-pathogen interactions, particularly focusing on immune responses to parasitic infections like Leishmania donovani. His work has explored how factors such as hyperlipidemia and membrane cholesterol influence host susceptibility and protection against Leishmania infection, with a publication dating back to 1997 on lipid peroxidation in visceral leishmaniasis. Ghosh also studies the role of specific immune cells and signaling pathways in host defense, examining B cells as antigen-presenting cells and the regulation of T cell differentiation by molecules like ICOS in response to infections such as Plasmodium chabaudi chabaudi AS. His research extends to understanding immune suppression mediated by tumor-associated macrophages and investigating hypersensitivity reactions to therapeutic inhibitors, linking them to specific HLA alleles. Ghosh's scholarship includes 39 publications and an h-index of 11, with collaborations at the University of Arkansas for Medical Sciences involving Jason S. Stumhofer, J. Craig Forrest, Mark Manzano, and Shana M. Owens.
Metrics
- h-index: 10
- Publications: 28
- Citations: 558
Positions
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Postdoctoral Researcher 2017–2022Stanford University Pediatrics ORCID
Selected Publications
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Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment (2025)
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p53 Controls Murine Gammaherpesvirus Latency and Prevents Infection-Associated IgH/c-Myc Translocations (2020)
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IL-17 Promotes Differentiation of Splenic LSK− Lymphoid Progenitors into B Cells following Plasmodium yoelii Infection (2017)
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An Atypical Splenic B Cell Progenitor Population Supports Antibody Production during Plasmodium Infection in Mice (2016)
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The Costimulatory Molecule ICOS Regulates Host Th1 and Follicular Th Cell Differentiation in Response to Plasmodium chabaudi chabaudi AS Infection (2015)
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Signaling Circuits and Regulation of Immune Suppression by Ovarian Tumor-Associated Macrophages (2015)
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Do You See What I See: Recognition of Protozoan Parasites by Toll-Like Receptors (2014)
Collaboration Network
Top Collaborators
- The Costimulatory Molecule ICOS Regulates Host Th1 and Follicular Th Cell Differentiation in Response to Plasmodium chabaudi chabaudi AS Infection
- Do You See What I See: Recognition of Protozoan Parasites by Toll-Like Receptors
- An Atypical Splenic B Cell Progenitor Population Supports Antibody Production during Plasmodium Infection in Mice
- IL-17 Promotes Differentiation of Splenic LSK− Lymphoid Progenitors into B Cells following Plasmodium yoelii Infection
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
Showing 5 of 6 shared publications
- The Costimulatory Molecule ICOS Regulates Host Th1 and Follicular Th Cell Differentiation in Response to Plasmodium chabaudi chabaudi AS Infection
- An Atypical Splenic B Cell Progenitor Population Supports Antibody Production during Plasmodium Infection in Mice
- The Costimulatory Molecule ICOS Regulates Host Th1 and Follicular Th Cell Differentiation in Response to Plasmodium chabaudi chabaudi AS Infection
- An Atypical Splenic B Cell Progenitor Population Supports Antibody Production during Plasmodium Infection in Mice
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- p53 Controls Murine Gammaherpesvirus Latency and Prevents Infection-Associated IgH/c-Myc Translocations
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- p53 Controls Murine Gammaherpesvirus Latency and Prevents Infection-Associated IgH/c-Myc Translocations
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- p53 Controls Murine Gammaherpesvirus Latency and Prevents Infection-Associated IgH/c-Myc Translocations
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- p53 Controls Murine Gammaherpesvirus Latency and Prevents Infection-Associated IgH/c-Myc Translocations
- Signaling Circuits and Regulation of Immune Suppression by Ovarian Tumor-Associated Macrophages
- Signaling Circuits and Regulation of Immune Suppression by Ovarian Tumor-Associated Macrophages
- An Atypical Splenic B Cell Progenitor Population Supports Antibody Production during Plasmodium Infection in Mice
- An Atypical Splenic B Cell Progenitor Population Supports Antibody Production during Plasmodium Infection in Mice
- An Atypical Splenic B Cell Progenitor Population Supports Antibody Production during Plasmodium Infection in Mice
- IL-17 Promotes Differentiation of Splenic LSK− Lymphoid Progenitors into B Cells following Plasmodium yoelii Infection
- p53 Controls Murine Gammaherpesvirus Latency and Prevents Infection-Associated IgH/c-Myc Translocations
- p53 Controls Murine Gammaherpesvirus Latency and Prevents Infection-Associated IgH/c-Myc Translocations
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