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Adenophages are an atypical macrophage population in exocrine glands sustained by ILC2-derived GM-CSF

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE280844 | GEO | 2025/10/27

REPOSITORIES: GEO

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Adenophages are an atypical macrophage population in exocrine glands sustained by ILC2-derived GM-CSF

Project description:Adenophages are an atypical macrophage population in exocrine glands sustained by ILC2-derived GM-CSF

| PRJNA1180895 | ENA

Developing exocrine glands harbour a distinct macrophage population that is maintained by ILC2 derived GM-CSF [scRNA-seq]

Project description:Granulocyte-macrophage colony-stimulating factor (GM-CSF) has a non-redundant role in the emergence and maintenance of alveolar macrophages (AMs). However, its role in steady-state myelopoiesis outside the lung is largely unexplored. We discovered a strong signal of GM-CSF production by type 2 innate lymphoid cells (ILC2s) in the developing salivary glands (SG). ILC2 derived GM-CSF fosters the development of a hitherto undescribed phagocyte subset, which we named adenophages. Detailed analysis focusing on phenotypic and transcriptional profiling revealed that adenophages represent a non-canonical macrophage subset displaying shared aspects of both, macrophages and dendritic cells. We found them to be homogenously distributed across the SG, but always forming a niche-triad with GM-CSF producing ILC2s and myoepithelial cells. Importantly, adenophages were present throughout all analyzed exocrine glands such as lacrimal glands and mammary glands, and were also identified in human SG, indicating a conserved role in exocrine glands across species.

2025-10-28 | GSE280842 | GEO

Developing exocrine glands harbour a distinct macrophage population that is maintained by ILC2 derived GM-CSF [bulk RNA-seq]

2025-10-28 | GSE280841 | GEO

Developing exocrine glands harbour a distinct macrophage population that is maintained by ILC2 derived GM-CSF [CD45 scRNA-seq]

2025-10-28 | GSE280882 | GEO

Developing exocrine glands harbour a distinct macrophage population that is maintained by ILC2 derived GM-CSF [scRNA-seq]

Project description:Developing exocrine glands harbour a distinct macrophage population that is maintained by ILC2 derived GM-CSF [scRNA-seq]

| PRJNA1180904 | ENA

Developing exocrine glands harbour a distinct macrophage population that is maintained by ILC2 derived GM-CSF [bulk RNA-seq]

Project description:Developing exocrine glands harbour a distinct macrophage population that is maintained by ILC2 derived GM-CSF [bulk RNA-seq]

| PRJNA1180900 | ENA

Developing exocrine glands harbour a distinct macrophage population that is maintained by ILC2 derived GM-CSF [CD45 scRNA-seq]

Project description:Developing exocrine glands harbour a distinct macrophage population that is maintained by ILC2 derived GM-CSF [CD45 scRNA-seq]

| PRJNA1180966 | ENA

AMFR drives allergic asthma development by promoting alveolar macrophage-derived GM-CSF production.

Project description:Alveolar macrophages (AMs) are specialized tissue-resident macrophages that orchestrate the immune response in allergic inflammation and asthma. However, what signals direct AMs to cross talk with other immune cells remains unclear. Here, we report that autocrine motility factor receptor (AMFR), an endoplasmic reticulum-resident E3 ubiquitin ligase, is upregulated in AMs of asthma and is critical for this condition. AMFR deficiency significantly decreased allergy-induced T helper 2 (Th2) and eosinophilic inflammation, with less granulocyte-macrophage colony-stimulating factor (GM-CSF) production in AMs. Mechanistically, following thymic stromal lymphopoietin (TSLP) stimulation, AMFR associated directly with cytokine-inducible SH2-containing protein (CIS), induced the ubiquitination of Lys48-linked polyubiquitination of CIS, and consequently blocked the inhibitory effect of CIS on signal transducer and activator of transcription 5 (STAT5) phosphorylation and the downstream pathway activation in AMs. In conclusion, our results demonstrate that AMFR serves a crucial role in promoting inflammation in asthma through regulating AM function, and may emerge as a new potential drug target for asthma therapy.

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Cxxc Finger Protein 1 Positively Regulates GM-CSF-Derived Macrophage Phagocytosis Through Csf2rα-Mediated Signaling.

Project description:Macrophages have a defensive function against bacteria through phagocytosis and the secretion of cytokines. Histone modifications play an essential role in macrophage functions. Here, we report that Cxxc finger protein 1 (CFP1), a key component of the SETD1 histone methyltransferase complex, promoted the phagocytic and bactericidal activity of GM-CSF-derived macrophages. CFP1-deficient mice were more susceptible to bacterial infection due to the decreased expression of Csf2rα, a subunit of the GM-CSF receptor essential for inflammation and alveolar macrophage development, through the loss of H3K4 modifications in the promoter of the Csf2rα gene. In addition, the lung tissues of CFP1-deficient mice exhibited spontaneous inflammatory symptoms, including both the infiltration of inflammatory cells and the accumulation of surfactant phospholipids and proteins. Furthermore, we showed that Csf2rα and PU.1 can partially rescue the defects in phagocytosis and in the intracellular killing of bacteria. Collectively, our data highlight the importance of CFP1 in the phagocytic and bactericidal activity of macrophages.

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GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury.

Project description:After kidney ischemia/reperfusion (I/R) injury, monocytes home to the kidney and differentiate into activated macrophages. Whereas proinflammatory macrophages contribute to the initial kidney damage, an alternatively activated phenotype can promote normal renal repair. The microenvironment of the kidney during the repair phase mediates the transition of macrophage activation from a proinflammatory to a reparative phenotype. In this study, we show that macrophages isolated from murine kidneys during the tubular repair phase after I/R exhibit an alternative activation gene profile that differs from the canonical alternative activation induced by IL-4-stimulated STAT6 signaling. This unique activation profile can be reproduced in vitro by stimulation of bone marrow-derived macrophages with conditioned media from serum-starved mouse proximal tubule cells. Secreted tubular factors were found to activate macrophage STAT3 and STAT5 but not STAT6, leading to induction of the unique alternative activation pattern. Using STAT3-deficient bone marrow-derived macrophages and pharmacologic inhibition of STAT5, we found that tubular cell-mediated macrophage alternative activation is regulated by STAT5 activation. Both in vitro and after renal I/R, tubular cells expressed GM-CSF, a known STAT5 activator, and this pathway was required for in vitro alternative activation of macrophages by tubular cells. Furthermore, administration of a neutralizing antibody against GM-CSF after renal I/R attenuated kidney macrophage alternative activation and suppressed tubular proliferation. Taken together, these data show that tubular cells can instruct macrophage activation by secreting GM-CSF, leading to a unique macrophage reparative phenotype that supports tubular proliferation after sterile ischemic injury.

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