# The role of CX3CR1+ CD4+ T cells during helminth infection

> **NIH NIH R21** · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · 2021 · $211,875

## Abstract

Parasitic helminths infect over 2 billion people worldwide. They cause significant morbidity and mortality in
developing areas of the world, especially among children. An effective vaccine against any type of human
helminth infections has been elusive, partly because there is a poor understanding of how to induce protective
immunity against these parasites. Parasitic helminths induce a CD4+ TH2 driven immune response. This
response is necessary not only to expel the parasite, but also to repair tissue damage caused by infection and
mitigate any further pathology resulting from chronic persistence. The development of an effective vaccine to
helminths may require a meticulous understanding of the mechanism of CD4+ memory T cell formation and
function. Certain subsets of CD4+ and CD8+ T cells will express the chemokine receptor CX3CR1 during
inflammation and infection. CX3CR1 expression on CD8+ T cells can help predict memory phenotypes during
viral infections. The role of CX3CR1+ CD4+ T cells during type-2 immune responses induced by helminth
infection is completely unknown. We have recently found that CX3CR1+ CD4+ T cells accumulate in the
tissues affected by helminth infections, but not in the draining lymph nodes. During Schistosoma mansoni
infection CX3CR1+ CD4+ T cells accumulate in the liver during granuloma formation. During Nippostrongylus
brasiliensis infection these cells rapidly accumulate in the lungs. The goal of this proposal is to further
characterize the phenotype and function of this population of CD4+ T cells, through two specific aims. In the
first Aim, we will test the hypothesis that CX3CR1+ CD4+ T cells from inflamed tissues during helminth
infection can differentiate into T follicular helper cells after trafficking to the spleen. In the second Aim, we will
determine if CX3CR1+ CD4+ T cells contribute to germinal center formation, antibody responses and host
protection against secondary infection. Overall, the study we propose will increase our understanding of
CD4+CX3CR1+ cells in the tissues of helminth infected mice, during a type-2 immune response. This
population of T cells is poorly understood and may be important for supporting antibody responses, parasite
expulsion, protective immunity and tissue repair. Utilizing genetic fate-mapping and conditional depletion
systems, we can thoroughly characterize their phenotype and function during helminth infections.

## Key facts

- **NIH application ID:** 10083698
- **Project number:** 5R21AI147359-02
- **Recipient organization:** NEW YORK UNIVERSITY SCHOOL OF MEDICINE
- **Principal Investigator:** Kamal Mohan Khanna
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $211,875
- **Award type:** 5
- **Project period:** 2020-01-10 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10083698

## Citation

> US National Institutes of Health, RePORTER application 10083698, The role of CX3CR1+ CD4+ T cells during helminth infection (5R21AI147359-02). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10083698. Licensed CC0.

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