# NIH grant: The impact of menstruation on tissue resident memory T cell durability (1R01HD116985-01A1) — retained record

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source: [us-gov-api](https://highsignal.app/data/us-gov-api) (us-gov-api:nih-reporter)  published 2026-06-23 00:00 ingested 2026-06-29 10:35

[original source ↗](https://reporter.nih.gov/project-details/1R01HD116985-01A1)

## retained text



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NIH grant 1R01HD116985-01A1: The impact of menstruation on tissue resident memory T cell durability
Institute: {'code': 'HD', 'abbreviation': 'NICHD', 'name': 'Eunice Kennedy Shriver National Institute of Child Health and Human Development', 'admin_org_id': '12500030', 'admin_funding_url': ''}. PI: Alison Swaims Kohlmeier. Award: $609863.
Start: 2026-06-23T00:00:00.
Abstract:
Although the vast majority of women and adolescent girls of reproductive age experience periodic menstruation,
how this immune-mediated tissue remodeling process compromises cellular immunity generated against
genitourinary pathogens, including Chlamydia trachomatis (C. trachomatis), is poorly understood. C. trachomatis
is the causative agent of one of the most costly and common bacterial sexually transmitted infections (STIs),
with the highest incidence occurring in women and adolescent girls of reproductive age. Genital chlamydial
infections can lead to severe diseases and health complications, including congenital transmissions, ectopic
pregnancies, infertility, and chronic pelvic pain. Moreover, chlamydial infections increase the risk of acquiring
more severe secondary infections. Taken together, these facts emphasize the critical need for an effective
vaccine to support mucosal immunity in the FRT. Memory T cells that become localized in the cervicovaginal
and uterine mucosa through a recent infection or from vaccination provide optimal immune protection against
chlamydial infections, leading to more rapid bacterial clearance and reducing disease severity. Therefore,
generating long-lived resident memory T cells in the reproductive tract mucosa that will recognize and respond
against C. trachomatis is a promising approach to strengthening immunity. Previous scientific research
investigations into understanding tissue-resident memory T cell durability demonstrate that local environmental
molecular signals can provide critical support that determines tissue-resident memory T cell development,
regionalization, and prolonged viability at sites such as the lung, skin, and gut. Yet, despite the fact that genital
chlamydial reinfections in women and adolescent girls of reproductive age are common and there is no available
vaccine, we have a very limited understanding of how menstruation alters the reproductive tract environment to
drive the depletion of pre-existing T cell immunity. Therefore, a major challenge for developing prophylactic
strategies, including vaccines that can prevent genital infections, is determining how to support long-lived and
durable tissue-resident memory T cells in the reproductive tract under menstrual cycle regulation. The goals of
our proposal are to acquire critical insights into the mechanism(s) by which menstruation regulates memory T
cell function and identify strategies that can support optimal memory T cell durability against chlamydial infections
in cervicovaginal and uterine tissues throughout this process.
```



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