# Regulation and function of B cells during malaria infection- Resubmission

> **NIH NIH R01** · UNIV OF ARKANSAS FOR MED SCIS · 2020 · $446,642

## Abstract

   
DESCRIPTION (provided by applicant): The protozoan parasite Plasmodium is the causative agent of malaria, which remains one of the most prominent public health challenges in the world today. Plasmodium-specific antibody responses are important for protecting against subsequent reinfections in humans and mice. However, while mice are protected after a single infection, protective immunity is slow to develop in humans due to the requirement of repeated infections for the generation of protective antibodies. Our long-term goal is to determine how protective antibody responses are generated and maintained in mice after Plasmodium infection, so that we can utilize this information to understand why antibody-mediated immunity is slow to develop in humans. Plasmodium-specific memory B cells are generated after infection in mice and humans; however, surprisingly little information is available regarding their specificity, phenotype, origin and affinity for malarial antigens. Our preliminary studies indicate that there are layers of heterogeneity within the memory B cell pool after Plasmodium infection and we hypothesize that this heterogeneity in the memory B cell pool contributes to functional diversity in a secondary infection. We propose to (Aim 1) characterize heterogeneous populations of memory B cells after P. yoelii 17X infection in mice and determine their origin. We will then (Aim 2) determine the function of distinct subsets of memory B cells after secondary infection. Additionally, our preliminary studies have identified two populations of memory T cells that express markers associated with follicular helper T cells. We propose to (Aim 3) determine if these populations of memory T cells are capable of differentiating into functional follicular helpe T cells that can support Ab production in a secondary infection and whether they are required for protection after challenge. To accomplish these goals we have developed innovative tools to track parasite- specific B cell responses at the cellular level utilizing parasites engineered to express hen egg-white lysozyme (HEL). Using HEL-specific transgenic B cells and a novel magnetic-bead based enrichment technique we can monitor and track the fate of antigen-specific B cells after infection with HEL expressing parasites. These innovative tools and approaches will provide valuable insight into understanding how protective immunity against Plasmodium is generated, is maintained, and functions in a secondary immune response and will identify key components involved in this process.

## Key facts

- **NIH application ID:** 9821179
- **Project number:** 5R01AI116653-05
- **Recipient organization:** UNIV OF ARKANSAS FOR MED SCIS
- **Principal Investigator:** Jason S Stumhofer
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $446,642
- **Award type:** 5
- **Project period:** 2015-12-04 → 2021-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9821179

## Citation

> US National Institutes of Health, RePORTER application 9821179, Regulation and function of B cells during malaria infection- Resubmission (5R01AI116653-05). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9821179. Licensed CC0.

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