ArticleArteriosclerosis, thrombosis, and vascular biology2013
Helix-loop-helix factor inhibitor of differentiation 3 regulates interleukin-5 expression and B-1a B cell proliferation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
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- The Role of B Lymphocyte Subsets in Adipose Tissue Development, Metabolism, and Aging.Comprehensive Physiology · 2022Article
- The why and how of adaptive immune responses in ischemic cardiovascular disease.Nature cardiovascular research · 2022Article
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- Heartbreakers or Healers? Innate Lymphoid Cells in Cardiovascular Disease and Obesity.Frontiers in immunology · 2022Review
- Screening Biomarkers for Systemic Lupus Erythematosus Based on Machine Learning and Exploring Their Expression Correlations With the Ratios of Various Immune Cells.Frontiers in immunology · 2022Article
- Friend or foe of innate lymphoid cells in inflammation-associated cardiovascular disease.Immunology · 2021Review
- Helix-Loop-Helix Factor Id3 (Inhibitor of Differentiation 3): A Novel Regulator of Hyaluronan-Mediated Adipose Tissue Inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Innate Lymphoid Cells and Myocardial Infarction.Frontiers in immunology · 2021Review
- Chemokine Receptor-6 Promotes B-1 Cell Trafficking to Perivascular Adipose Tissue, Local IgM Production and Atheroprotection.Frontiers in immunology · 2021Article
- B Lymphocytes and Adipose Tissue Inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2020Review
- 2019 Russell Ross Memorial Lecture in Vascular Biology: B Lymphocyte-Mediated Protective Immunity in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions.BMC immunology · 2019Article
- Inhibitor of DNA binding in heart development and cardiovascular diseases.Cell communication and signaling : CCS · 2019Review
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10 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveNatural immunity is emerging as an important mediator of protection from atherogenesis. Natural IgM antibodies that recognize oxidation-specific epitopes on low-density lipoprotein or phospholipids and the B-1a B cells that produce them attenuate atherosclerosis. We previously demonstrated that Apoe(-/-) mice globally deficient in the helix-loop-helix protein inhibitor of differentiation 3 (Id3) develop early diet-induced atherosclerosis. Furthermore, B cell-mediated attenuation of atherosclerosis in B cell-deficient mice was dependent on Id3. Here, we sought to determine whether Id3 regulates B-1a B cells and the natural antibodies that they produce and identify mechanisms mediating these effects. APPROACH AND
resultsMice lacking Id3 had significantly fewer B-1a B cells in the spleen and peritoneal cavity and reduced serum levels of the natural antibody E06. B cell-specific deletion of Id3 revealed that this effect was not because of the loss of Id3 in B cells. Interleukin (IL)-33 induced abundant, Id3-dependent IL-5 production in the recently identified innate lymphoid cell, the natural helper (NH) cell, but not Th2 or mast cells. In addition, delivery of IL-5 to Id3-deficient mice restored B-1a B cell proliferation. B-1a B cells were present in aortic samples also containing NH cells. Aortic NH cells produced IL-5, a B-1a B cell mitogen in response to IL-33 stimulation.
conclusionsThese studies are the first to identify NH and B-1a B cells in the aorta and provide evidence that Id3 is a key regulator of NH cell IL-5 production and B-1a B cell homeostasis.
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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.