# The role of CD40L in resistance to enteric infection

> **NIH NIH U01** · UNIVERSITY OF PENNSYLVANIA · 2022 · $552,706

## Abstract

Project Summary
The ability of recently activated T cells to express the cell surface molecule CD40L allows them to
communicate with other immune and non-immune populations. This molecule is of particular importance in the
gut to help control the parasitic infection caused by Cryptosporidium. Here we leverage a novel, natural mouse
model of Cryptosporidium to dissect the impact of the CD40-CD40L interaction in T cell-mediated resistance to
infection in the gut. In this model, WT mice (like humans) develop sterile immunity mediated by T cell
production of IFN-γ, but mice that lack CD40L mice (like humans) do not resolve infection. In addition,
treatment of chronically infected CD40L-deficient mice with soluble (s)CD40L results in rapid parasite
clearance. We will test if protective effect of CD40L may be explained by either I. its ability to promote T cell
responses essential for resistance and/or II. because CD40L directly activates EC to limit parasite growth. We
are uniquely equipped to utilize parasite transgenesis, combined with sophisticated genetic approaches to
define the key cellular interactions that allows CD40L to determine the outcome of an enteric infection.

## Key facts

- **NIH application ID:** 10470882
- **Project number:** 5U01AI163671-02
- **Recipient organization:** UNIVERSITY OF PENNSYLVANIA
- **Principal Investigator:** CHRISTOPHER A HUNTER
- **Activity code:** U01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $552,706
- **Award type:** 5
- **Project period:** 2021-08-17 → 2026-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10470882

## Citation

> US National Institutes of Health, RePORTER application 10470882, The role of CD40L in resistance to enteric infection (5U01AI163671-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10470882. Licensed CC0.

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