Artikel ; Online: Myeloid A20 is critical for alternative macrophage polarization and type-2 immune-mediated helminth resistance.
2024 Band 15, Seite(n) 1373745
Abstract: Background: Protective immunity against intestinal helminths requires induction of robust type-2 immunity orchestrated by various cellular and soluble effectors which promote goblet cell hyperplasia, mucus production, epithelial proliferation, and ... ...
| Abstract | Background: Protective immunity against intestinal helminths requires induction of robust type-2 immunity orchestrated by various cellular and soluble effectors which promote goblet cell hyperplasia, mucus production, epithelial proliferation, and smooth muscle contractions to expel worms and re-establish immune homeostasis. Conversely, defects in type-2 immunity result in ineffective helminth clearance, persistent infection, and inflammation. Macrophages are highly plastic cells that acquire an alternatively activated state during helminth infection, but they were previously shown to be dispensable for resistance to Methods: We use the in vivo mouse model A20myel-KO, characterized by the deletion of the potent anti-inflammatory factor A20 (TNFAIP3) specifically in the myeloid cells, the excessive type-1 cytokine production, and the development of spontaneous arthritis. We infect A20 Results: We show that proper macrophage polarization is essential for helminth clearance, and we identify A20 as an essential myeloid factor for the induction of type-2 immune responses against Conclusions: We hereby identify A20 as a critical myeloid factor for correct macrophage polarization and appropriate adaptive mucosal immunity in response to helminth and enteric bacterial infection. |
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| Mesh-Begriff(e) | Animals ; Mice ; Cytokines/metabolism ; Cytokines/immunology ; Disease Models, Animal ; Disease Resistance/genetics ; Disease Resistance/immunology ; Immunity, Innate ; Macrophage Activation/immunology ; Macrophages/immunology ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Cells/immunology ; Th2 Cells/immunology ; Trichuriasis/immunology ; Trichuris/immunology ; Tumor Necrosis Factor alpha-Induced Protein 3/immunology ; Tumor Necrosis Factor alpha-Induced Protein 3/genetics |
| Chemische Substanzen | Cytokines ; Tnfaip3 protein, mouse (EC 3.4.22.-) ; Tumor Necrosis Factor alpha-Induced Protein 3 (EC 3.4.19.12) |
| Sprache | Englisch |
| Erscheinungsdatum | 2024-04-12 |
| Erscheinungsland | Switzerland |
| Dokumenttyp | Journal Article ; Research Support, Non-U.S. Gov't |
| ZDB-ID | 2606827-8 |
| ISSN | 1664-3224 ; 1664-3224 |
| ISSN (online) | 1664-3224 |
| ISSN | 1664-3224 |
| DOI | 10.3389/fimmu.2024.1373745 |
| Datenquelle | MEDical Literature Analysis and Retrieval System OnLINE |
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