Academic Journal

Motherhood's Sentinels: Pregnancy Induces Tissue-Resident Memory T Cells to Curb Breast Cancer Growth.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Motherhood's Sentinels: Pregnancy Induces Tissue-Resident Memory T Cells to Curb Breast Cancer Growth.
Συγγραφείς: Sudhakaran M; Cancer Metabolism and Microenvironment Program, NCI-Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California., Kersten K; Cancer Metabolism and Microenvironment Program, NCI-Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California.
Πηγή: Cancer research [Cancer Res] 2026 Oct 15; Vol. 86 (20), pp. 5020-5022.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: American Association for Cancer Research Country of Publication: United States NLM ID: 2984705R Publication Model: Print Cited Medium: Internet ISSN: 1538-7445 (Electronic) Linking ISSN: 00085472 NLM ISO Abbreviation: Cancer Res Subsets: MEDLINE
Imprint Name(s): Publication: Baltimore, Md. : American Association for Cancer Research
Original Publication: Chicago [etc.]
Ιατρικοί όροι (MeSH): Breast Neoplasms*/immunology , Breast Neoplasms*/pathology , Memory T Cells*/immunology , CD8-Positive T-Lymphocytes*/immunology , Immunologic Memory*, Parity/immunology ; Female ; Pregnancy ; Animals ; Humans ; Mice
Περίληψη: Women who carry a pregnancy to term have long been known to have a reduced lifetime risk of breast cancer, yet the mechanisms underlying this protection remain poorly understood. Although parity-induced differentiation and hormonal remodeling of the mammary epithelium have been considered primary drivers of breast cancer protection, the contribution of immune adaptation has remained largely unexplored. In a recent issue of Nature Immunology, Hussain and colleagues identify pregnancy-induced tissue-resident memory-like (TRM-like) CD8+ T cells as key mediators of parity-associated breast cancer protection. The authors show that pregnancy establishes a nurturing niche in the mammary gland that supports the expansion of TRM-like cells through epithelial-derived IL15 and TGFβ and that depletion of these cells abolishes the cancer-protective effect of parity. Moreover, using therapeutic agents to enhance IL2Rβ signaling was sufficient to induce the expansion of breast cancer-protective TRM-like cells in nulliparous mice, raising the possibility that pregnancy's protective imprint could be pharmacologically induced. Given the established link between TRM cells and immune checkpoint blockade responsiveness in breast cancer, these findings also raise the possibility that pregnancy-induced TRM-like populations could be leveraged to improve immunotherapy outcomes. By linking physiologic developmental tissue remodeling to durable local immunosurveillance, this study expands current concepts of tissue-resident immunity and positions pregnancy as an immune-educating event with lasting consequences for breast cancer susceptibility.
(©2026 American Association for Cancer Research.)
Entry Date(s): Date Created: 20260810 Date Completed: 20261015 Latest Revision: 20261015
Update Code: 20261015
DOI: 10.1158/0008-5472.CAN-26-3367
PMID: 42574140
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1538-7445
DOI:10.1158/0008-5472.CAN-26-3367