# T cell homeostasis

> **NIH NIH R01** · UNIVERSITY OF MINNESOTA · 2020 · $378,474

## Abstract

Project Summary
 It has become clear that a subset of T lymphocytes, called “resident memory” T cells (TRM), is
tremendously important for preventing infection by pathogenic microbes through “barrier” tissues, such
as the skin, lungs, gut and reproductive tract. These T cells directly kill infected cells, or recruit other
immune cells to assist in protecting these tissues. In contrast to the well-studied “migratory” memory T
cells (which transit through the blood and lymph in order to hunt for sites of infection), resident memory T
cells do not leave the barrier tissues. Since these cells can be so valuable for protective immunity,
directed generation of TRM provides an exciting opportunity to enhance vaccines. Similarly, TRM-like cells
in tumors have also been found to correlate with a good prognosis. At the same time, TRM are not always
a good thing – they are associated with various autoimmune and inflammatory responses (for example
psoriasis), hence there are some occasions when it would be valuable to displace TRM from tissues.
Interestingly, we recently found that another population of T cells, called “germinal center follicular
helpers” (GC-TFH) have some of the same properties as TRM – although these cells live in lymphoid
tissues like the lymph node, not barrier tissues.
 However, the molecular “rules” that determine whether a T cell will be resident versus migratory
are unclear – existing data is confusing and contradictory. The fact that some factors are coordinately
expressed in various resident T cell populations started us thinking that there may be core molecular
mechanisms that distinguish all the different resident T cell types from all the migratory T cell types. This
proposal explores that hypothesis.
 We focus on a panel of factors that are differentially expressed by migratory and resident T cells,
but the function of which is incompletely understood. Through sophisticated genetic tools, we will
explore what these factors do in numerous situations (involving different T cell populations and diverse
infectious models). This involves experiments where we can induce increased or decreased expression
of these factors at the timing of our choice (e.g. when cells first arrive in the gut – or 30 days later), and in
the location of our choice (e.g. just the cells in the skin, not the cells in the blood).

## Key facts

- **NIH application ID:** 9971428
- **Project number:** 5R01AI038903-25
- **Recipient organization:** UNIVERSITY OF MINNESOTA
- **Principal Investigator:** STEPHEN C JAMESON
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $378,474
- **Award type:** 5
- **Project period:** 1996-07-01 → 2022-02-10

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9971428

## Citation

> US National Institutes of Health, RePORTER application 9971428, T cell homeostasis (5R01AI038903-25). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9971428. Licensed CC0.

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