Tissue-resident macrophages can derive from yolk sac macrophages (YS-Macs), fetal liver monocytes (FL-MOs), or adult bone-marrow monocytes (BM-MOs). The relative capacity of these precursors to colonize a niche, self-maintain, and perform tissue-specific functions is unknown. We simultaneously transferred traceable YS-Macs, FL-MOs, and BM-MOs into the empty alveolar macrophage (AM) niche of neonatal Csf2rb(-/-) mice. All subsets produced AMs, but in competition preferential outgrowth of FL-MOs was observed, correlating with their superior granulocyte macrophage-colony stimulating factor (GM-CSF) reactivity and proliferation capacity. When transferred separately, however, all precursors efficiently colonized the alveolar niche and generated AMs that were transcriptionally almost identical, self-maintained, and durably prevented alveolar proteinosis. Mature liver, peritoneal, or colon macrophages could not efficiently colonize the empty AM niche, whereas mature AMs could. Thus, precursor origin does not affect the development of functional self-maintaining tissue-resident macrophages and the plasticity of the mononuclear phagocyte system is largest at the precursor stage.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.immuni.2016.02.017 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Deriving human intestinal organoids with functional tissue-resident macrophages all from pluripotent stem cells.
Cell Mol Gastroenterol Hepatol
December 2024
Division of Developmental Biology; Division of Endocrinology; Center for Stem Cell and Organoid Medicine, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229-3039. Electronic address:
Background & Aims: Organs of the gastrointestinal tract contain tissue-resident immune cells that function during tissue development, homeostasis, and disease. However, most published human organoid model systems lack resident immune cells, thus limiting their potential as disease avatars. For example, human intestinal organoids (HIOs) derived from pluripotent stem cells contain epithelial and various mesenchymal cell types but lack immune cells.
View Article and Find Full Text PDFExacerbation of pulmonary fibrosis following acute lung injury via activin-A production by recruited alveolar macrophages.
J Thorac Dis
November 2024
Shanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Background: Acute respiratory distress syndrome (ARDS) is a complicated pathological cascade process of excessive pulmonary inflammation and alveolar epithelial cell apoptosis that results in respiratory dysfunction and failure. Some cases of ARDS can result in a more severe state of pulmonary fibrosis, referred to as postinjury lung fibrosis. The mortality and incidence rate of ARDS are high, particularly when it leads to continuing alveolar and interstitial fibrosis, which requires urgent treatment and appropriate management.
View Article and Find Full Text PDFInteractions between the developing heart and the embryonic immune system are essential for proper cardiac development and maintaining homeostasis, with disruptions linked to various diseases. While human pluripotent stem cell (hPSC)-derived organoids are valuable models for studying human organ function, they often lack critical tissue-resident immune cells. Here, we introduce an advanced human heart assembloid model, termed hHMA (human heart-macrophage assembloid), which fully integrates autologous cardiac tissue- resident macrophages (MPs) with pre-existing human heart organoids (hHOs).
View Article and Find Full Text PDFICAM1 gingival fibroblasts modulate periodontal inflammation to mitigate bone loss.
Front Immunol
December 2024
Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Tissue-resident fibroblasts are heterogeneous and provide an endogenous source of cytokines that regulate immunologic events in many osteolytic diseases. Identifying distinct inflammatory fibroblast subsets and conducting mechanistic studies are critical for understanding disease pathogenesis and precision therapeutics, which is poorly explored in periodontitis. Here, we surveyed published single-cell datasets for fibroblast-specific analysis and show that Intercellular Adhesion Molecule-1 (ICAM1) expression selectively defines a fibroblast subset that exhibits an inflammatory transcriptional profile associated with nuclear factor-κB (NF-κB) pathway.
View Article and Find Full Text PDFIL-17A/CEBPβ/OPN/LYVE-1 axis inhibits anti-tumor immunity by promoting tumor-associated tissue-resident macrophages.
Cell Rep
December 2024
Key Laboratory of Organ Regeneration & Transplantation of the Ministry of Education, The First Hospital of Jilin University, Changchun, China; National-local Joint Engineering Laboratory of Animal Models for Human Diseases, Jilin University, Changchun, China; International Center of Future Science, Jilin University, Changchun, China. Electronic address:
Tumor-associated macrophages (TAMs) are a critical component of the immunosuppressive tumor microenvironment, comprising monocyte-derived macrophages (MDM-TAMs) and tissue-resident macrophages (TRM-TAMs). Here, we discovered that TRM-TAMs mediate the pro-tumor effects of interleukin (IL)-17A and that IL-17A-driven tumor progression requires tumor cell production of osteopontin (OPN). Mechanistically, we identified CEBPβ as a transcription factor downstream of IL-17A in tumor cells and LYVE-1 as an OPN receptor on TRM-TAMs.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!