Abstract
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-4Rα) 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.
Original language | English |
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Pages (from-to) | 1064-1081.e10 |
Journal | Immunity |
Volume | 56 |
Issue number | 5 |
DOIs | |
State | Published - May 9 2023 |
Keywords
- GATA6
- Litomosoides sigmodontis
- alternatively activated macrophages
- converting cavity macrophage
- filariasis
- helminth
- interleukin 13
- interleukin 4
- serous cavities
- strain-dependent immunity