IL-33 stimulation of human lung mast cells for 2 and 24 hours
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE314641 | GEO | 2026/03/19
REPOSITORIES: GEO
Similar Datasets
Project description:Interleukin-33 (IL-33) is elevated in afflicted tissues of patients with mast cell-dependent chronic allergic diseases. Based on its acute effects on mouse mast cells (MCs), IL-33 is thought to play a role in the pathogenesis of allergic disease through MC activation. However, the manifestations of chronic IL-33 exposure on human MC function, which best reflect the conditions associated with chronic allergic disease, are unknown. We now find that long-term exposure of human and mouse MCs to IL-33 results in a substantial reduction of MC activation in response to antigen. This reduction required >72 h exposure to IL-33 for onset and 1-2 wk for reversion following IL-33 removal. This hypo-responsive phenotype was determined to be a consequence of MyD88-dependent attenuation of signaling processes necessary for MC activation including antigen-mediated calcium mobilization and cytoskeletal reorganization; potentially as a consequence of down-regulation of the expression of PLCg1 and Hck. These findings suggest that IL-33 may play a protective, rather than a causative role in MC activation under chronic conditions and, furthermore, reveal regulated plasticity in the MC activation phenotype. The ability to down-regulate MC activation in this manner may provide alternative approaches for treatment of MC-driven disease. Mouse bone marrow-derived mast cells treated with IL3 or IL3+IL33. 6 replicates each.
2013-02-06 | E-GEOD-39382 | biostudies-arrayexpress
Project description:Expression of CD25 in human lung mast cells and its regulation by IL-33
| PRJNA1392371 | ENA
Project description:Interleukin-33 (IL-33) is elevated in afflicted tissues of patients with mast cell-dependent chronic allergic diseases. Based on its acute effects on mouse mast cells (MCs), IL-33 is thought to play a role in the pathogenesis of allergic disease through MC activation. However, the manifestations of chronic IL-33 exposure on human MC function, which best reflect the conditions associated with chronic allergic disease, are unknown. We now find that long-term exposure of human and mouse MCs to IL-33 results in a substantial reduction of MC activation in response to antigen. This reduction required >72 h exposure to IL-33 for onset and 1-2 wk for reversion following IL-33 removal. This hypo-responsive phenotype was determined to be a consequence of MyD88-dependent attenuation of signaling processes necessary for MC activation including antigen-mediated calcium mobilization and cytoskeletal reorganization; potentially as a consequence of down-regulation of the expression of PLCg1 and Hck. These findings suggest that IL-33 may play a protective, rather than a causative role in MC activation under chronic conditions and, furthermore, reveal regulated plasticity in the MC activation phenotype. The ability to down-regulate MC activation in this manner may provide alternative approaches for treatment of MC-driven disease.
2013-02-06 | GSE39382 | GEO
Project description:Mast cells are tissue resident granulocytes which are most abundant at the interface between tissues and the external environment, such as around blood vessels, in the skin or mucosal surfaces in the lungs and gut. Pathologically they are involved in allergic reactions and anaphylaxis, however they may also play protective roles in responses to some infections, particularly to pathogenic helminths. Mast cells also express high levels of the IL-33 receptor, which like TLRs, activates Myd88 dependent signalling pathways to drive de novo cytokine production in mast cells.IL-33 is a member of the IL-1 family known to stimulate a number of immune cell types including mast cells. IL-33 is a strong activator of de novo cytokine production in mast cells without inducing degranulation, although it has also been shown to synergise with other signals to promote degranulation. Bone Marrow-Derived Mast cells (BMMCs) were cultured as described previously [27]. Briefly, bone marrow was flushed in PBS and the cells pelleted by centrifugation. Cells were cultured at 1 million cells per ml in RPMI 1640 supplemented with 10% FBS (Biosera/Labtech), 5 mM l‐Glutamine (GIBCO Life Technologies), 100 U/ml Penicillin (GIBCO Life Technologies), 100 μg/ml Streptomycin (GIBCO Life Technologies), 25 mM HEPES (Lonza), 1 mM sodium pyruvate (Lonza), 1X nonessential amino acids (Lonza), 50 μM 2‐mercaptoethanol and 30 ng/ml IL‐3 (PeproTech). Cells were passaged twice per week and used between passage 12 and 16. 4 independent BMMC cultures were either stimulated with 10 ng/ml IL-33 for 48 hours or left unstimulated, followed by single shot LC-MS analysis.
2023-03-11 | PXD033759 | Pride
Project description:CD25 (IL-2R) can be expressed on the surface of immune cells in the absence of other chains of the interleukin-2 receptor (IL-2R), which are indispensable for IL-2 signaling. We identified two novel mast cell subsets, characterized by the differential expression of surface CD25, and by the ability to produce different cytokines and to proliferate, both in vitro and in vivo. We provide evidence that functional differences between the two mast cell populations were dependent on CD25 itself, which directly modulated mast cell proliferation and responses in vivo. These effects were completely independent from IL-2 or the expression of the other chains of the high-affinity IL-2R, indicating an autonomous and previously unappreciated role for CD25 in regulating cell functions. Similar results were also obtained in dendritic cells, which are known to express CD25 but to be unresponsive to IL-2. Our findings indicate a general role for CD25 in contexts where IL-2 signaling is not involved, and may have important implications for all mast cell-related diseases, including mastocytosis, where CD25 is aberrantly expressed on pathogenic mast cells. Total mRNA of FACS-sorted CD25pos and CD25neg populations of primary bone marrow-derived mast cells (BMMCs) was extracted and subjected to by multiparallel sequencing.
2014-08-03 | E-GEOD-52502 | biostudies-arrayexpress
Project description:CD25 (IL-2R) can be expressed on the surface of immune cells in the absence of other chains of the interleukin-2 receptor (IL-2R), which are indispensable for IL-2 signaling. We identified two novel mast cell subsets, characterized by the differential expression of surface CD25, and by the ability to produce different cytokines and to proliferate, both in vitro and in vivo. We provide evidence that functional differences between the two mast cell populations were dependent on CD25 itself, which directly modulated mast cell proliferation and responses in vivo. These effects were completely independent from IL-2 or the expression of the other chains of the high-affinity IL-2R, indicating an autonomous and previously unappreciated role for CD25 in regulating cell functions. Similar results were also obtained in dendritic cells, which are known to express CD25 but to be unresponsive to IL-2. Our findings indicate a general role for CD25 in contexts where IL-2 signaling is not involved, and may have important implications for all mast cell-related diseases, including mastocytosis, where CD25 is aberrantly expressed on pathogenic mast cells.
2014-08-03 | GSE52502 | GEO
Project description:Mast cells respond to acute and chronic exposure to IL-33 by differing the expression of their receptors, cytokines and proteases. We aim to characterize the distinct acute and chronic responses of mast cells to IL-33 by analyzing hCBMC expression profile of pro- and anti- inflammatory mediators.
2024-10-03 | GSE224089 | GEO
Project description:Synergy of signals often causes cells to exhibit stronger physiological responses, especially immune cells. Here we reported that priming of interleukin-33 (IL-33) played a crucial role in the subsequent response of mast cells to ATP. Judging from the levels of cytokines and chemokines, the synergy of IL-33 priming and ATP stimulation was as high as 65%. At the entire transcriptional level, high synergy was also observed. This provided evidence supporting the sequential release of IL-33 and ATP derived from stromal cells on mast cells in vivo. Likewise, the upregulation of numerous cytokines and chemokines provided enormous support for mast cells to regulate antiviral immunity.
2026-03-13 | GSE298699 | GEO
Project description:Synergy of signals often causes cells to exhibit stronger physiological responses, especially immune cells. Here we reported that priming of interleukin-33 (IL-33) played a crucial role in the subsequent response of mast cells to ATP. Judging from the levels of cytokines and chemokines, the synergy of IL-33 priming and ATP stimulation was as high as 64%. At the entire transcriptional level, high synergy was also observed. This provided evidence supporting the sequential release of IL-33 and ATP derived from stromal cells on mast cells in vivo. Likewise, the upregulation of numerous cytokines and chemokines provided enormous support for mast cells to regulate antiviral immunity.
2026-03-13 | GSE263663 | GEO
Project description:Synergy of signals often causes cells to exhibit stronger physiological responses, especially immune cells. Here we reported that priming of interleukin-33 (IL-33) played a crucial role in the subsequent response of mast cells with Gq signaling. Judging from the levels of cytokines and chemokines, the synergy of IL-33 priming and Gq signaling activation was as high as 53%. At the entire transcriptional level, high synergy was also observed. This provided evidence supporting the sequential release of IL-33 and Gq signaling activator derived from stromal cells on mast cells in vivo. Likewise, the upregulation of numerous cytokines and chemokines provided enormous support for mast cells to regulate antiviral immunity.
2026-03-13 | GSE263664 | GEO