# Mechanisms by which CD74 Contributes to Traumatic Brain Injury

> **NIH NIH R01** · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · 2021 · $399,083

## Abstract

Project Summary/ Abstract
Traumatic brain injury (TBI), and the ensuing post-traumatic behavioral and
neurological syndromes, are serious clinical problems. Approximately 5 million
people in the U.S. are living with the chronic consequences of TBI, and optimal
treatment strategies are lacking. We have discovered that specific components of
the immune system contribute to neuropathology after a TBI. More specifically,
we have discovered that CD74, a protein that functions via unique mechanisms
that distinctly contribute to either the innate or the adaptive immune response, can
be manipulated to improve neurodegeneration and behavioral outcomes after TBI.
Our proposal is based on three primary observations:
1) Our preliminary data implicating full-length CD74 signaling via macrophage
migration inhibitory factor (MIF)-binding in the astrocytic response to TBI; 2) Our
data indicating that depleting full-length CD74 or antagonizing the proteolytic
cleavage product(s) of CD74, class II invariant peptide (CLIP), are anti-
inflammatory and neuroprotective after TBI; 3) Recent evidence from human
clinical TBI patients and experimental TBI in animal models, showing strong
evidence for an adaptive immune response, potentially including autoimmunity.
Taken together, these studies are important because: A) they will assess the
distinct contributions of CD74 to the innate and adaptive immune responses
following TBI; B) they will distinguish between the unique mechanisms of CD74
that contribute to TBI-induced neuropathology and post-traumatic behavioral
syndromes; and C) they will determine if targeting specific components of CD74
might be a potential therapeutic strategy following TBI.

## Key facts

- **NIH application ID:** 10241518
- **Project number:** 5R01NS104282-04
- **Recipient organization:** TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR
- **Principal Investigator:** M. Karen Newell Rogers
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $399,083
- **Award type:** 5
- **Project period:** 2019-09-01 → 2023-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10241518

## Citation

> US National Institutes of Health, RePORTER application 10241518, Mechanisms by which CD74 Contributes to Traumatic Brain Injury (5R01NS104282-04). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10241518. Licensed CC0.

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