Theobald, H.; Bejarano, D. A.; Katzmarski, N.; Haub, J.; Schulte-Schrepping, J.; Yu, J.; Bassler, K.; Ament, A. L.; Osei-Sarpong, C.; Piattini, F.; Vornholz, L.; T’Jonck, W.; Györfi, A. H.; Hayer, H.; Yu, X.; Sheoran, S.; Al Jawazneh, A.; Chakarov, S.; Haendler, K.; Brown, G. D.; Williams, D. L.; Bosurgi, L.; Distler, J. H. W.; Ginhoux, F.; Ruland, J.; Beyer, M. D.; Greter, M.; Bain, C. C.; Vazquez-Armendariz, A. I.; Kopf, M.; Schultze, J. L.; Schlitzer, A.: Apolipoprotein E controls Dectin-1-dependent development of monocyte-derived alveolar macrophages upon pulmonary β-glucan-induced inflammatory adaptation. In: Nature immunology. 2024, vol. 25, 994-1006.
Online-Ausgabe in bonndoc: https://hdl.handle.net/20.500.11811/13563
@article{handle:20.500.11811/13563,
author = {{H. Theobald} and {D. A. Bejarano} and {N. Katzmarski} and {J. Haub} and {J. Schulte-Schrepping} and {J. Yu} and {K. Bassler} and {A. L. Ament} and {C. Osei-Sarpong} and {F. Piattini} and {L. Vornholz} and {W. T’Jonck} and {A. H. Györfi} and {H. Hayer} and {X. Yu} and {S. Sheoran} and {A. Al Jawazneh} and {S. Chakarov} and {K. Haendler} and {G. D. Brown} and {D. L. Williams} and {L. Bosurgi} and {J. H. W. Distler} and {F. Ginhoux} and {J. Ruland} and {M. D. Beyer} and {M. Greter} and {C. C. Bain} and {A. I. Vazquez-Armendariz} and {M. Kopf} and {J. L. Schultze} and {A. Schlitzer}},
title = {Apolipoprotein E controls Dectin-1-dependent development of monocyte-derived alveolar macrophages upon pulmonary β-glucan-induced inflammatory adaptation},
publisher = {Springer Nature},
year = 2024,
month = apr,

journal = {Nature immunology},
volume = 2024, vol. 25,
pages = 994--1006,
note = {The lung is constantly exposed to the outside world and optimal adaptation of immune responses is crucial for efficient pathogen clearance. However, mechanisms that lead to lung-associated macrophages' functional and developmental adaptation remain elusive. To reveal such mechanisms, we developed a reductionist model of environmental intranasal β-glucan exposure, allowing for the detailed interrogation of molecular mechanisms of pulmonary macrophage adaptation. Employing single-cell transcriptomics, high-dimensional imaging and flow cytometric characterization paired with in vivo and ex vivo challenge models, we reveal that pulmonary low-grade inflammation results in the development of apolipoprotein E (ApoE)-dependent monocyte-derived alveolar macrophages (ApoE+CD11b+AMs). ApoE+CD11b+ AMs expressed high levels of CD11b, ApoE, Gpnmb and Ccl6, were glycolytic, highly phagocytic and produced large amounts of interleukin-6 upon restimulation. Functional differences were cell intrinsic, and myeloid cell-specific ApoE ablation inhibited Ly6c+ monocyte to ApoE+CD11b+AM differentiation dependent on macrophage colony-stimulating factor secretion, promoting ApoE+CD11b+AM cell death and thus impeding ApoE+CD11b+AM maintenance. In vivo, β-glucan-elicited ApoE+CD11b+ AMs limited the bacterial burden of Legionella pneumophilia after infection and improved the disease outcome in vivo and ex vivo in a murine lung fibrosis model. Collectively these data identify ApoE+CD11b+AMs generated upon environmental cues, under the control of ApoE signaling, as an essential determinant for lung adaptation enhancing tissue},
url = {https://hdl.handle.net/20.500.11811/13563}
}

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