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Determining the role of T cells in controlling endometrial dynamics and mammalian fertility

Award Number: F30HD121243
ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 12/01/2026
PERIOD OF PERFORMANCE END DATE: 11/30/2030

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Determining the role of T cells in controlling endometrial dynamics and mammalian fertility - PROJECT SUMMARY/ABSTRACT The uterine endometrium undergoes a coordinated and cyclic turnover that is unlike any other mammalian tissue. Whereas most epithelial surfaces shed their apical surface in a progressive manner, the uterus undergoes a periodic synchronous turnover. The murine endometrium undergoes a 20-40% reduction in size every four days. The remarkable rate and persistence of this process throughout much of a female lifespan raises questions about the fundamental mechanisms that regulate this process and their implications on reproductive and gynecological health. Interestingly, the healthy, non-pregnant endometrium, in both mice and humans, consists of a variety of immune cells. However, the specific functions of these immune cells and if they contribute to uterine turnover remains unclear. Preliminary results demonstrate that a population of CD4+ T cells periodically enter the endometrium and are activated locally in a TCR-dependent manner. Eliminating these cells leads to prolonged time to endometrial degradation. The overall hypothesis of the proposed work is that T cells specific for endometrial antigens serve as key mediators of controlled endometrial turnover. This proposal seeks to determine whether T cell mediated endometrial turnover is driven by self-antigens (Aim 1), define the mechanisms by which T cells promote endometrial turnover (Aim 2), and understand the implications of endometrial T cells in mammalian fertility and gynecologic disease (Aim 3). To address aim one, other possible sources of antigen will be evaluated by assessing the activation state and endometrial turnover dynamics in microbiome deficient mice as well as mice without endogenous retroviruses. To understand the mechanisms of endometrial T cells in driving turnover we will integrate quantitative multiplexed imaging as well as genetic models to identify key effector proteins and cell types involved in tissue breakdown. Finally, using defined inflammatory insults and genetically engineered mouse models lacking various components of the immune system will show how the dysregulation or removal of endometrial T cells affects reproductive cycle dynamics and fertility. The proposed project will define a local and controlled autoimmune T cell response that contributes to homeostatic breakdown of the uterus. The findings of this research have the potential to reshape our understanding of endometrial biology and tissue immune interactions, with implications in mammalian fertility, autoimmunity, and gynecological diseases of the endometrium.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $43,325 )
2026	2026	PRESIDENT AND FELLOWS OF HARVARD COLLEGE	25 SHATTUCK ST	BOSTON	MA	02115	SUFFOLK	USA	Child Health and Human Development Extramural Research	001	1	9/11/2026	NEW	$0
2026	2026	PRESIDENT AND FELLOWS OF HARVARD COLLEGE	25 SHATTUCK ST	BOSTON	MA	02115	SUFFOLK	USA	Child Health and Human Development Extramural Research	000	1	9/11/2026	NEW	$43,325
														Subtotal = $43,325

Grand Total All Awards = $43,325

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Determining the role of T cells in controlling endometrial dynamics and mammalian fertility

Award Number: F30HD121243

ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 12/01/2026

PERIOD OF PERFORMANCE END DATE: 11/30/2030

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