# Mobilization of tissue-resident lymphocytes during secondary infection

> **NIH NIH R21** · RBHS-NEW JERSEY MEDICAL SCHOOL · 2020 · $229,158

## Abstract

T cells play a critical role in eliminating pathogens and the generation of memory T cells is an
important component in protection from secondary infection. Memory T cells can be broadly
divided into two groups based on their location, those that are capable of circulating throughout
the body and those that are lodged in tissues, poised to respond rapidly to secondary infection.
Tissue-resident memory T cells (Trm) cells remain in the tissue and are not replenished by
circulating cells after infection is resolved. Circulating T cells are often not sufficient to protect
from secondary infection; therefore, it is of significant interest to determine how to maximize the
number and functionality of Trm cells as they are critical for robust tissue-specific immunity. Only
a small number of microbes need to breach the mucosal surface to initiate disease; however, the
mechanism by which established Trm populations detect and migrate to new areas of infection
remains unexplored. Our earlier work, using the intestinal bacterial pathogen Yersinia
pseudotuberculosis (Yptb), identified two distinct CD8+ Trm populations in the intestine that are
differentiated by their expression of the integrin CD103. CD103neg Trm cells preferentially localize
to lymphocyte clusters that form around areas of infection and limit pathogen replication, but
dissipate after infection is resolved. CD103neg CD4+ and CD8+ Trm populations are also abundant
in other tissues, but their respective roles in tissue-specific immunity remain poorly understood.
We hypothesize the diversity in the tissue-resident lymphocyte population underlies a functional
heterogeneity, with the CD103neg subset of lymphocytes capable of localized migration in
response to tissue-specific signals that alert them to a pathogenic insult and forms the basis for
lymphocyte cluster formation around new areas of infection during secondary challenge. These
studies will utilize photoconversion to mark tissue-resident cells and allowing us to track cellular
migration during homeostasis and intestinal infection. We will leverage this technique to address
fundamental gaps in our knowledge of Trm biology including: (1) how Trm diversity relates to
functional outcomes during secondary infection and (2) the identification of signals generated by
the tissue in response to infection that drive Trm mobilization and pathogen control. These
experiments have the potential to significantly advance our understanding of tissue-resident
lymphocyte biology and how immunization strategies can be tailored to improve Trm functionality.

## Key facts

- **NIH application ID:** 10056391
- **Project number:** 1R21AI148900-01A1
- **Recipient organization:** RBHS-NEW JERSEY MEDICAL SCHOOL
- **Principal Investigator:** Tessa Bergsbaken
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $229,158
- **Award type:** 1
- **Project period:** 2020-05-25 → 2022-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10056391

## Citation

> US National Institutes of Health, RePORTER application 10056391, Mobilization of tissue-resident lymphocytes during secondary infection (1R21AI148900-01A1). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10056391. Licensed CC0.

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