| First Author | Finlay CM | Year | 2023 |
| Journal | Immunity | Volume | 56 |
| Issue | 5 | Pages | 1064-1081.e10 |
| PubMed ID | 36948193 | Mgi Jnum | J:335619 |
| Mgi Id | MGI:7481875 | Doi | 10.1016/j.immuni.2023.02.016 |
| Citation | Finlay CM, et al. (2023) T helper 2 cells control monocyte to tissue-resident macrophage differentiation during nematode infection of the pleural cavity. Immunity 56(5):1064-1081.e10 |
| abstractText | The recent revolution in tissue-resident macrophage biology has resulted largely from murine studies performed in C57BL/6 mice. Here, using both C57BL/6 and BALB/c mice, we analyze immune cells in the pleural cavity. Unlike C57BL/6 mice, naive tissue-resident large-cavity macrophages (LCMs) of BALB/c mice failed to fully implement the tissue-residency program. Following infection with a pleural-dwelling nematode, these pre-existing differences were accentuated with LCM expansion occurring in C57BL/6, but not in BALB/c mice. While infection drove monocyte recruitment in both strains, only in C57BL/6 mice were monocytes able to efficiently integrate into the resident pool. Monocyte-to-macrophage conversion required both T cells and interleukin-4 receptor alpha (IL-4Ralpha) signaling. The transition to tissue residency altered macrophage function, and GATA6(+) tissue-resident macrophages were required for host resistance to nematode infection. Therefore, during tissue nematode infection, T helper 2 (Th2) cells control the differentiation pathway of resident macrophages, which determines infection outcome. |
