Receptors, Interleukin-1 Type I
"Receptors, Interleukin-1 Type I" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
An interleukin-1 receptor subtype that is involved in signaling cellular responses to INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The binding of this receptor to its ligand causes its favorable interaction with INTERLEUKIN-1 RECEPTOR ACCESSORY PROTEIN and the formation of an activated receptor complex.
MeSH Number(s)
D12.776.543.750.705.852.420.300.500
D23.050.301.264.035.697
D23.101.100.110.697
Concept/Terms
Receptors, Interleukin-1 Type I- Receptors, Interleukin-1 Type I
- Receptors, Interleukin 1 Type I
- Interleukin-1 Receptors Type I
- Interleukin 1 Receptors Type I
- CD121a Antigens
- Interleukin-1 Receptor Type I
- Interleukin 1 Receptor Type I
- Receptor Type I, Interleukin-1
- Receptor Type I, Interleukin 1
- Antigens, CDw121a
- CDw121a Antigens
Below are MeSH descriptors whose meaning is more general than "Receptors, Interleukin-1 Type I".
- Chemicals and Drugs [D]
- Amino Acids, Peptides, and Proteins [D12]
- Proteins [D12.776]
- Membrane Proteins [D12.776.543]
- Receptors, Cell Surface [D12.776.543.750]
- Receptors, Immunologic [D12.776.543.750.705]
- Receptors, Cytokine [D12.776.543.750.705.852]
- Receptors, Interleukin [D12.776.543.750.705.852.420]
- Receptors, Interleukin-1 [D12.776.543.750.705.852.420.300]
- Receptors, Interleukin-1 Type I [D12.776.543.750.705.852.420.300.500]
- Biological Factors [D23]
- Antigens [D23.050]
- Antigens, Surface [D23.050.301]
- Antigens, Differentiation [D23.050.301.264]
- Antigens, CD [D23.050.301.264.035]
- Receptors, Interleukin-1 Type I [D23.050.301.264.035.697]
- Biological Markers [D23.101]
- Antigens, Differentiation [D23.101.100]
- Antigens, CD [D23.101.100.110]
- Receptors, Interleukin-1 Type I [D23.101.100.110.697]
Below are MeSH descriptors whose meaning is more specific than "Receptors, Interleukin-1 Type I".
This graph shows the total number of publications written about "Receptors, Interleukin-1 Type I" by people in Harvard Catalyst Profiles by year, and whether "Receptors, Interleukin-1 Type I" was a major or minor topic of these publication.
To see the data from this visualization as text,
click here.
| Year | Major Topic | Minor Topic | Total |
|---|
| 2004 | 0 | 1 | 1 |
| 2008 | 1 | 0 | 1 |
| 2011 | 1 | 0 | 1 |
| 2012 | 1 | 2 | 3 |
| 2013 | 3 | 0 | 3 |
| 2014 | 0 | 1 | 1 |
| 2015 | 1 | 4 | 5 |
| 2016 | 0 | 2 | 2 |
| 2019 | 1 | 1 | 2 |
| 2020 | 0 | 1 | 1 |
Below are the most recent publications written about "Receptors, Interleukin-1 Type I" by people in Profiles.
-
Interleukin-1ß inhibits normal hematopoietic expansion and promotes acute myeloid leukemia progression via the bone marrow niche. Cytotherapy. 2020 03; 22(3):127-134.
-
Ptpn6 inhibits caspase-8- and Ripk3/Mlkl-dependent inflammation. Nat Immunol. 2020 01; 21(1):54-64.
-
IL1R1 is required for celastrol's leptin-sensitization and antiobesity effects. Nat Med. 2019 04; 25(4):575-582.
-
Cell-Type-Specific Interleukin 1 Receptor 1 Signaling in the Brain Regulates Distinct Neuroimmune Activities. Immunity. 2019 02 19; 50(2):317-333.e6.
-
IL-1R and MyD88 signalling in CD4+ T cells promote Th17 immunity and atherosclerosis. Cardiovasc Res. 2018 01 01; 114(1):180-187.
-
Glucose-dependent insulinotropic peptide secretion is induced by inflammatory stimuli in an interleukin-1-dependent manner in mice. Diabetes Obes Metab. 2016 11; 18(11):1147-1151.
-
Allergic skin sensitization promotes eosinophilic esophagitis through the IL-33-basophil axis in mice. J Allergy Clin Immunol. 2016 11; 138(5):1367-1380.e5.
-
Increased Myeloid Cell Production and Lung Bacterial Clearance in Mice Exposed to Cigarette Smoke. Am J Respir Cell Mol Biol. 2016 Mar; 54(3):424-35.
-
Enhanced susceptibility to seizures modulated by high interleukin-1ß levels during early life malnutrition. Dev Neurobiol. 2016 10; 76(10):1150-9.
-
Neuroinflammation impairs adaptive structural plasticity of dendritic spines in a preclinical model of Alzheimer's disease. Acta Neuropathol. 2016 Feb; 131(2):235-246.