The Induction of Inflammation by Dectin-1 In Vivo Is Dependent on Myeloid Cell Programming and the Progression of Phagocytosis
| العنوان: | The Induction of Inflammation by Dectin-1 In Vivo Is Dependent on Myeloid Cell Programming and the Progression of Phagocytosis |
|---|---|
| المؤلفون: | Kate Liddiard, Inês Faro-Trindade, Gordon D. Brown, David L. Williams, Jacqueline U. McDonald, Matti Kimberg, Philip R. Taylor, Marcela Rosas |
| المصدر: | The Journal of Immunology. 181:3549-3557 |
| بيانات النشر: | The American Association of Immunologists, 2008. |
| سنة النشر: | 2008 |
| مصطلحات موضوعية: | beta-Glucans, Myeloid, Phagocytosis, Immunology, Nerve Tissue Proteins, Inflammation, Biology, Mice, Immune system, Candida albicans, medicine, Animals, Immunology and Allergy, Macrophage, Lectins, C-Type, Myeloid Cells, Receptor, Mice, Knockout, Macrophages, Pattern recognition receptor, Membrane Proteins, Dendritic Cells, Dendritic cell, Cell biology, medicine.anatomical_structure, Mycoses, medicine.symptom |
| الوصف: | Dectin-1 is the archetypal signaling, non-Toll-like pattern recognition receptor that plays a protective role in immune defense to Candida albicans as the major leukocyte receptor for β-glucans. Dectin-1-deficiency is associated with impaired recruitment of inflammatory leukocytes and inflammatory mediator production at the site of infection. In this study, we have used mice to define the mechanisms that regulate the dectin-1-mediated inflammatory responses. Myeloid cell activation by dectin-1 is controlled by inherent cellular programming, with distinct macrophage and dendritic cell populations responding differentially to the engagement of this receptor. The inflammatory response is further modulated by the progression of the phagocytosis, with “frustrated phagocytosis” resulting in dramatically augmented inflammatory responses. These studies demonstrate that dectin-1 in isolation is sufficient to drive a potent inflammatory response in a context-dependent manner. This has implications for the mechanism by which myeloid cells are activated during fungal infections and the processes involved in the therapeutic manipulation of the immune system via exogenous dectin-1 stimulation or blockade. |
| تدمد: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.181.5.3549 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::cf1f2f3499768eb765afd47881645d75 https://doi.org/10.4049/jimmunol.181.5.3549 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....cf1f2f3499768eb765afd47881645d75 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15506606 00221767 |
|---|---|
| DOI: | 10.4049/jimmunol.181.5.3549 |