# The role of tissue-resident T cells in resolving inflammation of the human oral mucosa

> **NIH NIH R56** · FRED HUTCHINSON CANCER CENTER · 2022 · $615,312

## Abstract

Project Summary
Tissue destruction and bone loss occur due to uncontrolled and progressing inflammation within gingival
tissue. Resolution of inflammation is necessary to return to a homeostatic state and to initiate
reparative/regenerative functions within mucosal tissues. We examined chronically inflamed gingival tissues to
determine if T cells with anti-inflammatory function (regulatory T cells; Treg) and tissue-repair function (IL-17
and IL-22 secreting T cells; Th17/22) are lost or preserved during inflammation. We found that Treg and
Th17/22 CD4 T cell populations were still intact in the inflamed gingiva suggesting that there is a retained
intrinsic ability to resolve inflammation. We now propose to interrogate different mechanisms that could
interfere with Th17/22 and Treg promoted resolution of inflammation. Of note, some IL-17 is critical to maintain
barrier immunity, while excess IL-17 drives tissue pathology, thus the presence Th17 cells must be interpreted
carefully and in context of the T cell population. We consider and propose to test several different possibilities:
tissue damaging effector T cells may counteract ongoing repair efforts, Treg and Th17/22 functions may not be
properly elicited in the inflamed gingiva and repair efforts may be actively suppressed by APCs. The goal of
our proposed experiments is to gain a better understanding of the immunological mechanisms that perpetuate
a state of inflammation and prevent resolution of inflammation in chronically inflamed gingiva. Identifying these
immunological mechanisms is relevant as it will help provide insight to ultimately allow for selective therapeutic
targeting of immune cell subsets to treat chronically inflamed oral tissues.

## Key facts

- **NIH application ID:** 10625076
- **Project number:** 1R56DE032009-01
- **Recipient organization:** FRED HUTCHINSON CANCER CENTER
- **Principal Investigator:** Douglas Raymond Dixon
- **Activity code:** R56 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $615,312
- **Award type:** 1
- **Project period:** 2022-08-08 → 2025-08-07

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10625076

## Citation

> US National Institutes of Health, RePORTER application 10625076, The role of tissue-resident T cells in resolving inflammation of the human oral mucosa (1R56DE032009-01). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10625076. Licensed CC0.

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