Match tier
Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-10-09
K
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Kara A. O’Neal investigates the immune response to malaria, specifically focusing on the parasite *Plasmodium yoelii* in mouse models. Her research examines the role of various immune mediators, including Interleukin-10 (IL-10), Interferon-gamma (IFN-γ), and Interleukin-12 (IL-12), in controlling infection. Studies have explored how deficiencies in these cytokines impact the course of the disease, often finding enhanced control of early infection in IL-10-deficient mice, independent of IFN-γ, IL-12, and humoral responses. O'Neal's work also delves into the function of specific immune cells, such as B-lymphocytes and CD4+ T cells, and their contribution to the host's defense mechanisms. Her collaborations include researchers from the University of Arkansas for Medical Sciences and the National Center for Toxicological Research.
Metrics
- h-index: 2
- Publications: 5
- Citations: 9
Selected Publications
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Early enhanced control of Plasmodium yoelii infection in IL-10-deficient mice is independent of IFN-γ, IL-12, and the humoral response (2026)
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Early enhanced control of Plasmodium yoelii infection in IL-10–deficient mice is independent of IFN-γ, IL-12, and the humoral response (2026)
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Bhlhe40 limits early IL-10 production from CD4 + T cells during Plasmodium yoelii 17X infection (2023)
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ICOS Expression Is Required for Maintenance but Not the Formation of Germinal Centers in the Spleen in Response to Plasmodium yoelii Infection (2022)
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ICOS expression is required for maintenance but not the formation of germinal centers in the spleen in response to P. yoelii infection (2021)
Collaboration Network
Top Collaborators
Jason S. Stumhofer
University of Arkansas for Medical Sciences
5 shared publications
In database
- ICOS Expression Is Required for Maintenance but Not the Formation of Germinal Centers in the Spleen in Response to Plasmodium yoelii Infection
- Bhlhe40 limits early IL-10 production from CD4 + T cells during Plasmodium yoelii 17X infection
- ICOS expression is required for maintenance but not the formation of germinal centers in the spleen in response to P. yoelii infection
- Early enhanced control of Plasmodium yoelii infection in IL-10–deficient mice is independent of IFN-γ, IL-12, and the humoral response
- Early enhanced control of Plasmodium yoelii infection in IL-10-deficient mice is independent of IFN-γ, IL-12, and the humoral response
Camille L. Foscue
University of Arkansas for Medical Sciences
3 shared publications
In database
- ICOS Expression Is Required for Maintenance but Not the Formation of Germinal Centers in the Spleen in Response to Plasmodium yoelii Infection
- Bhlhe40 limits early IL-10 production from CD4 + T cells during Plasmodium yoelii 17X infection
- ICOS expression is required for maintenance but not the formation of germinal centers in the spleen in response to P. yoelii infection
Sheldon L. Zeltner
University of Arkansas for Medical Sciences
3 shared publications
In database
- Bhlhe40 limits early IL-10 production from CD4 + T cells during Plasmodium yoelii 17X infection
- Early enhanced control of Plasmodium yoelii infection in IL-10–deficient mice is independent of IFN-γ, IL-12, and the humoral response
- Early enhanced control of Plasmodium yoelii infection in IL-10-deficient mice is independent of IFN-γ, IL-12, and the humoral response
Leah E. Latham
University of Arkansas for Medical Sciences
2 shared publications
In database
- ICOS Expression Is Required for Maintenance but Not the Formation of Germinal Centers in the Spleen in Response to Plasmodium yoelii Infection
- ICOS expression is required for maintenance but not the formation of germinal centers in the spleen in response to P. yoelii infection
Enatha Ntirandekura
University of Arkansas for Medical Sciences
2 shared publications
In database
- ICOS Expression Is Required for Maintenance but Not the Formation of Germinal Centers in the Spleen in Response to Plasmodium yoelii Infection
- ICOS expression is required for maintenance but not the formation of germinal centers in the spleen in response to P. yoelii infection
Meghan D. Jones
University of Arkansas for Medical Sciences
2 shared publications
In database
- Early enhanced control of Plasmodium yoelii infection in IL-10–deficient mice is independent of IFN-γ, IL-12, and the humoral response
- Early enhanced control of Plasmodium yoelii infection in IL-10-deficient mice is independent of IFN-γ, IL-12, and the humoral response
Alison Gouch
University of Arkansas for Medical Sciences
2 shared publications
In database
- Early enhanced control of Plasmodium yoelii infection in IL-10–deficient mice is independent of IFN-γ, IL-12, and the humoral response
- Early enhanced control of Plasmodium yoelii infection in IL-10-deficient mice is independent of IFN-γ, IL-12, and the humoral response
Jeanette M. Ramos
University of Arkansas for Medical Sciences
1 shared publication
In database
- Early enhanced control of Plasmodium yoelii infection in IL-10-deficient mice is independent of IFN-γ, IL-12, and the humoral response
Similar Researchers
Based on overlapping research topics
Sheldon L. Zeltner
University of Arkansas for Medical Sciences
Host-Pathogen Interactions
Immune Response and Inflammation
Disease Models, Animal
Alison R. Gouch
University of Arkansas for Medical Sciences
Host-Pathogen Interactions
Immune Response and Inflammation
Disease Models, Animal
Bernabe Mercado
University of Arkansas for Medical Sciences
Host-Pathogen Interactions
Immune Response and Inflammation
Disease Models, Animal
Jessica I. Gann
University of Arkansas for Medical Sciences
Host-Pathogen Interactions
Immune Response and Inflammation
Disease Models, Animal
Lin‐Xi Li
University of Arkansas for Medical Sciences
Host-Pathogen Interactions
Immune Response and Inflammation
Disease Models, Animal
Marli S.P. Azevedo
National Center for Toxicological Research
Host-Pathogen Interactions
Immune Response and Inflammation
Disease Models, Animal