ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Ca2+ Signaling but Not Store-Operated Ca2+ Entry Is Required for the Function of Macrophages and Dendritic Cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
67 citing papers in PubMed.
- Store-operated calcium signaling modulators improve a dendritic cell-based vaccine against melanoma.Oncoimmunology · 2026Article
- CRAC channels as targets for immunotherapy.Current opinion in immunology · 2026Review
- Article
- Intravital calcium imaging of meningeal macrophages reveals niche-specific dynamics and aberrant responses to brain hyperexcitability.bioRxiv : the preprint server for biology · 2025Article
- Article
- Dietary targeting of TRPM8 rewires macrophage immunometabolism reducing colitis severity.Cell death & disease · 2025Article
- Metal-ion-chelating phenylalanine nanostructures reverse immune dysfunction and sensitize breast tumour to immune checkpoint blockade.Nature nanotechnology · 2024Article
- Role of STIM1 in stretch-induced signaling in human airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- STIM2 is involved in the regulation of apoptosis and the cell cycle in normal and malignant monocytic cells.Molecular oncology · 2024Article
- Synthetic Biology Meets CaCells · 2024Review
- TRPV1 modulated NLRP3 inflammasome activation via calcium in experimental subarachnoid hemorrhage.Aging · 2024Article
- Tmem178 Negatively Regulates IL-1β Production Through Inhibition of the NLRP3 Inflammasome.Arthritis & rheumatology (Hoboken, N.J.) · 2024Article
- Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells.Science advances · 2023Article
- Adipose-specific deletion of the cation channel TRPM7 inhibits TAK1 kinase-dependent inflammation and obesity in male mice.Nature communications · 2023Article
- LDL delivery of microbial small RNAs drives atherosclerosis through macrophage TLR8.Nature cell biology · 2022Article
- ORAI3 is dispensable for store-operated Ca2+ entry and immune responses by lymphocytes and macrophages.The Journal of general physiology · 2022Article
- Lysophosphatidylcholine induces adenosine release from macrophages via TRPM7-mediated mitochondrial activation.Purinergic signalling · 2022Article
- Toll-like receptor 4 activation enhances Orai1-mediated calcium signal promoting cytokine production in spinal astrocytes.Cell calcium · 2022Article
- Efferocytosis requires periphagosomal CaNature communications · 2022Article
- Vaccine adjuvants to engage the cross-presentation pathway.Frontiers in immunology · 2022Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Store-operated Ca(2+) entry (SOCE) through Ca(2+) release-activated Ca(2+) (CRAC) channels is essential for immunity to infection. CRAC channels are formed by ORAI1 proteins in the plasma membrane and activated by stromal interaction molecule (STIM)1 and STIM2 in the endoplasmic reticulum. Mutations in ORAI1 and STIM1 genes that abolish SOCE cause severe immunodeficiency with recurrent infections due to impaired T cell function. SOCE has also been observed in cells of the innate immune system such as macrophages and dendritic cells (DCs) and may provide Ca(2+) signals required for their function. The specific role of SOCE in macrophage and DC function, as well as its contribution to innate immunity, however, is not well defined. We found that nonselective inhibition of Ca(2+) signaling strongly impairs many effector functions of bone marrow-derived macrophages and bone marrow-derived DCs, including phagocytosis, inflammasome activation, and priming of T cells. Surprisingly, however, macrophages and DCs from mice with conditional deletion of Stim1 and Stim2 genes, and therefore complete inhibition of SOCE, showed no major functional defects. Their differentiation, FcR-dependent and -independent phagocytosis, phagolysosome fusion, cytokine production, NLRP3 inflammasome activation, and their ability to present Ags to activate T cells were preserved. Our findings demonstrate that STIM1, STIM2, and SOCE are dispensable for many critical effector functions of macrophages and DCs, which has important implications for CRAC channel inhibition as a therapeutic strategy to suppress pathogenic T cells while not interfering with myeloid cell functions required for innate immunity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.