# Unmasking the Immunomodulatory Roles of CD7 Signaling

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 2024 · $611,046

## Abstract

PROJECT SUMMARY/ABSTRACT
This NIAID R01 proposal describes the framework in which Wan-Lin Lo, Ph.D., will address the signaling
properties and physiological function of CD7 in T cells in her independent laboratory at the University of Utah
School of Medicine. While previous studies have treated CD7 as an inessential costimulatory molecule, the
preliminary results in this proposal suggest that CD7 supports T cell receptor (TCR) signaling and effector
functions: CD7 may function as a major PI3K-recruiting scaffold protein for the TCR in a ligand-independent way
and as a costimulatory receptor that lowers the TCR activation threshold. Dr. Lo envisions that CD7 is a novel
immunoregulatory target for the modulation of T cell function in infections, cancers, and autoimmune diseases.
The overall goals of this proposal are to characterize the mechanisms used by CD7 to facilitate T cell
differentiation during infection and to explore the possibility of targeting CD7 to enhance or mitigate T cell effector
function. The first goal will examine the influences of CD7-involved signaling in T cells during acute and chronic
viral infection at the proteomic, transcriptomic, and epigenetic levels, with the hypothesis that CD7 amplifies
proximal TCR signaling, stabilizes TCR:peptide–major histocompatibility complex interactions, and enhances T
cell responses to weak ligands. The second goal will define altered T cell fates in the absence of CD7 during
acute and chronic viral infection to test the hypothesis that CD7-involved signaling is essential to promote antiviral
T cell effector function, and that an optimal level of CD7 signaling is required to prevent T cell exhaustion due to
CD7 hyperreactivity or to avoid T cell unresponsiveness due to the absence of CD7. The objective of this study
is to address the current roadblocks to immunomodulatory therapies (i.e., T cell exhaustion and autoimmune
toxicities). The focuses of this proposal are highly relevant to the mission of NIAID, and will enhance our
understanding of the signaling mechanisms underlying T cell fate decisions during infection, especially the
inherent, characteristic proteomic adaptations and epigenetic reprogramming that reinforce T cell identities.
Ultimately, this work will aid the design and development of therapeutics to target CD7, and potentiate future
studies to assess how CD7-modulated T cell functional adaptation may be regulated in various disease settings.

## Key facts

- **NIH application ID:** 10891386
- **Project number:** 5R01AI175301-02
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **Principal Investigator:** Wan-Lin Lo
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $611,046
- **Award type:** 5
- **Project period:** 2023-07-20 → 2028-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10891386

## Citation

> US National Institutes of Health, RePORTER application 10891386, Unmasking the Immunomodulatory Roles of CD7 Signaling (5R01AI175301-02). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10891386. Licensed CC0.

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