{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Finlay CM"],"funding":["NIAID NIH HHS","Medical Research Council","Wellcome Trust","Biotechnology and Biological Sciences Research Council"],"pagination":["1064-1081.e10"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7616141"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["56(5)"],"pubmed_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<sup>+</sup> 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."],"journal":["Immunity"],"pubmed_title":["T helper 2 cells control monocyte to tissue-resident macrophage differentiation during nematode infection of the pleural cavity."],"pmcid":["PMC7616141"],"funding_grant_id":["MR/K01207X/1","106898/A/15/Z","MR/W018748/1","MR/K01207X/2","106898","BB/T014482/1","R37 AI049653"],"pubmed_authors":["Konkel JE","Kaymak I","Ruckerl D","Randolph GJ","Finlay CM","Boon L","Morrison A","Zhang L","Allen JE","Chan BHK","Chenery A","MacDonald AS","Houlder EL","Ajendra J","Parkinson JE","Dickie BR","Hepworth MR","Murtuza Baker S"],"additional_accession":[]},"is_claimable":false,"name":"T helper 2 cells control monocyte to tissue-resident macrophage differentiation during nematode infection of the pleural cavity.","description":"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<sup>+</sup> 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.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 May","modification":"2026-06-02T22:12:21.018Z","creation":"2024-10-18T19:32:14.789Z"},"accession":"S-EPMC7616141","cross_references":{"pubmed":["36948193"],"doi":["10.1016/j.immuni.2023.02.016"]}}