| First Author | Hanasoge Somasundara AV | Year | 2021 |
| Journal | Cell Rep | Volume | 37 |
| Issue | 10 | Pages | 110099 |
| PubMed ID | 34879282 | Mgi Jnum | J:320927 |
| Mgi Id | MGI:6881816 | Doi | 10.1016/j.celrep.2021.110099 |
| Citation | Hanasoge Somasundara AV, et al. (2021) Parity-induced changes to mammary epithelial cells control NKT cell expansion and mammary oncogenesis. Cell Rep 37(10):110099 |
| abstractText | Pregnancy reprograms mammary epithelial cells (MECs) to control their responses to pregnancy hormone re-exposure and carcinoma progression. However, the influence of pregnancy on the mammary microenvironment is less clear. Here, we used single-cell RNA sequencing to profile the composition of epithelial and non-epithelial cells in mammary tissue from nulliparous and parous female mice. Our analysis indicates an expansion of gammadelta natural killer T-like immune cells (NKTs) following pregnancy and upregulation of immune signaling molecules in post-pregnancy MECs. We show that expansion of NKTs following pregnancy is due to elevated expression of the antigen-presenting molecule CD1d on MECs. Loss of CD1d expression on post-pregnancy MECs, or overall lack of activated NKTs, results in mammary oncogenesis. Collectively, our findings illustrate how pregnancy-induced changes modulate the communication between MECs and the immune microenvironment and establish a causal link between pregnancy, the immune microenvironment, and mammary oncogenesis. |
