# The role of CD163L1 in CD8+ T cells

> **NIH NIH R21** · CORNELL UNIVERSITY · 2024 · $199,152

## Abstract

Project Summary / Abstract
Following infection, naïve CD8+ T cells differentiate into effector or memory T cells, which help to eliminate
pathogens and maintain long-term immunity. Despite decades of research, it is still not clear why some naïve
CD8+ T cells become effectors and die, whereas others survive and become long-lived memory cells. The
canonical model posits that a single lineage of CD8+ T cells undergoes phenotypic diversification after
stimulation. However, our published work and preliminary data show that there are separate lineages of CD8+
T cells (fetal-derived and adult-derived) in the starting population, which are made during distinct windows of
development and differentiate along different pathways during infection. This model suggests that the division
of labor within the CD8+ T cell compartment is mediated by distinct ontogenetic lineages, similar to
subpopulations of B cells (B1a, B1b, B2), which have unique functional capabilities. However, unlike the B cell
field, the T cell field lacks a useful marker to identify fetal- and adult-derived CD8+ T cells in adult mice, and we
still do not fully understand the underlying basis for their altered behavior. Based on our preliminary data and
published findings, we have identified a scavenger receptor (CD163L1) that is specifically expressed on fetal-
derived CD8+ T cells and contributes to their more rapid innate-like functions. In Aim 1, we will establish whether
CD163L1 is a marker for fetal-derived CD8+ T cells. In Aim 2, we will examine how CD163L1 alters the functions
of CD8+ T cells. Our proposal is expected to open up new avenues of research and advance our conceptual
understanding of the CD8+ T cell response to infection.

## Key facts

- **NIH application ID:** 10738771
- **Project number:** 5R21AI167858-02
- **Recipient organization:** CORNELL UNIVERSITY
- **Principal Investigator:** ANDREW W GRIMSON
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $199,152
- **Award type:** 5
- **Project period:** 2022-11-10 → 2025-10-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10738771

## Citation

> US National Institutes of Health, RePORTER application 10738771, The role of CD163L1 in CD8+ T cells (5R21AI167858-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10738771. Licensed CC0.

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