# Protective role of Clec7a/dectin-1 in CNS autoimmunity

> **NIH NIH R01** · DUKE UNIVERSITY · 2022 · $401,008

## Abstract

PROJECT SUMMARY/ABSTRACT
 Multiple sclerosis (MS) is considered to be a T cell-mediated autoimmune disease, and the relationship
between initial innate immune activity and neurodegeneration is still poorly understood. In this proposed project,
we aim to elucidate how the novel protective role of dectin-1, a C-type lectin receptor (CLR), is exerted through
crosstalk of myeloid cells infiltrated in the central nervous system (CNS) and CNS-resident cells in experimental
autoimmune encephalomyelitis (EAE) and cuprizone-induced demyelination (CID) models. Dectin-1 has been
one of the most intensively studied innate immune receptors, detecting fungal cell wall to induce inflammation.
However, we recently found that dectin-1 is a protective molecule in EAE, and the protective role of dectin-1 in
neuroinflammation has not been defined. In particular, the role of dectin-1 in MS/EAE is entirely unknown. Our
preliminary data also strongly suggested that endogenous molecules, expressed at least on astrocytes, trigger
the protective role of dectin-1.
 The goal of this project is to delineate how innate immune activities lead to neuroprotection in EAE. Based
on our preliminary data, our central hypothesis is: Myeloid cells sense endogenous inflammatory cues through
dectin-1 to mediate crosstalk between the immune system and CNS that promotes neuroprotection. This study
will contribute to a growing body of evidence that dectin-1 has importance beyond the context of fungal infection.
We advance this emerging understanding by identifying a new protective mechanism of Dectin-1, specifically in
the setting of CNS autoimmunity and neurodegeneration. This project will provoke consideration of dectin-1 and
its effector functions beyond the context of infection to provide potential novel targets for therapeutic intervention
in neuroinflammatory disorders.

## Key facts

- **NIH application ID:** 10312130
- **Project number:** 5R01NS120417-02
- **Recipient organization:** DUKE UNIVERSITY
- **Principal Investigator:** Mari L. Shinohara
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $401,008
- **Award type:** 5
- **Project period:** 2020-12-15 → 2025-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10312130

## Citation

> US National Institutes of Health, RePORTER application 10312130, Protective role of Clec7a/dectin-1 in CNS autoimmunity (5R01NS120417-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10312130. Licensed CC0.

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