Product: IL1 beta Antibody
Catalog: AF5103
Source: Rabbit
Application: WB, IHC, IF/ICC, ELISA(peptide)
Reactivity: Human, Mouse, Rat
Prediction: Horse, Rabbit
Mol.Wt.: 30 kD(precursor),17kD(mature); 31kD(Calculated).
Uniprot: P01584
RRID: AB_2837589

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 100ul $280 In stock
 200ul $350 In stock

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Product Info

WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500, ELISA(peptide) 1:20000-1:40000
*The optimal dilutions should be determined by the end user.

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Horse(80%), Rabbit(100%)
IL1 beta Antibody detects endogenous levels of total IL1 beta.
Cite Format: Affinity Biosciences Cat# AF5103, RRID:AB_2837589.
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


Catabolin; H1; IL 1; IL 1 beta; IL-1 beta; IL1 BETA; IL1B; IL1B_HUMAN; IL1F2; Interleukin 1 beta; Interleukin-1 beta; OAF; OTTHUMP00000162031; Preinterleukin 1 beta; Pro interleukin 1 beta;


P01584 IL1B_HUMAN:

Expressed in activated monocytes/macrophages (at protein level).

IL-1 production is generally thought to be associated with inflammation, but it has also been shown to be expressed during kidney development, thymocyte differentiation and cartilage degradation. IL-1 plays a critical role in the regulation of immune response and inflammation, acting as an activator of T and B lymphocytes and natural killer (NK) cells.



Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P01584 As Substrate

Site PTM Type Enzyme
Y140 Phosphorylation
S200 Phosphorylation
S269 Phosphorylation

Research Backgrounds


Potent proinflammatory cytokine. Initially discovered as the major endogenous pyrogen, induces prostaglandin synthesis, neutrophil influx and activation, T-cell activation and cytokine production, B-cell activation and antibody production, and fibroblast proliferation and collagen production. Promotes Th17 differentiation of T-cells. Synergizes with IL12/interleukin-12 to induce IFNG synthesis from T-helper 1 (Th1) cells.


Activation of the IL1B precursor involves a CASP1-catalyzed proteolytic cleavage. Processing and secretion are temporarily associated.

Subcellular Location:

Cytoplasm>Cytosol. Lysosome. Secreted>Extracellular exosome. Secreted.
Note: The precursor is cytosolic. In response to inflammasome-activating signals, such as ATP for NLRP3 inflammasome or bacterial flagellin for NLRC4 inflammasome, cleaved and secreted. IL1B lacks any known signal sequence and the pathway(s) of its secretion is(are) not yet fully understood (PubMed:24201029). On the basis of experimental results, several unconventional secretion mechanisms have been proposed. 1. Secretion via secretory lysosomes: a fraction of CASP1 and IL1B precursor may be incorporated, by a yet undefined mechanism, into secretory lysosomes that undergo Ca(2+)-dependent exocytosis with release of mature IL1B (PubMed:15192144). 2. Secretory autophagy: IL1B-containing autophagosomes may fuse with endosomes or multivesicular bodies (MVBs) and then merge with the plasma membrane releasing soluble IL1B or IL1B-containing exosomes (PubMed:24201029). However, autophagy impacts IL1B production at several levels and its role in secretion is still controversial. 3. Secretion via exosomes: ATP-activation of P2RX7 leads to the formation of MVBs containing exosomes with entrapped IL1B, CASP1 and other inflammasome components. These MVBs undergo exocytosis with the release of exosomes. The release of soluble IL1B occurs after the lysis of exosome membranes (By similarity). 4. Secretion by microvesicle shedding: activation of the ATP receptor P2RX7 may induce an immediate shedding of membrane-derived microvesicles containing IL1B and possibly inflammasome components. The cytokine is then released in the extracellular compartment after microvesicle lysis (PubMed:11728343). 5. Release by translocation through permeabilized plasma membrane. This may occur in cells undergoing pyroptosis due to sustained activation of the inflammasome (By similarity). These mechanisms may not be not mutually exclusive.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Expressed in activated monocytes/macrophages (at protein level).

Subunit Structure:

Monomer. In its precursor form, weakly interacts with full-length MEFV; the mature cytokine does not interact at all. Interacts with integrins ITGAV:ITGBV and ITGA5:ITGB1; integrin-binding is required for IL1B signaling.


Belongs to the IL-1 family.

Research Fields

· Cellular Processes > Cell growth and death > Necroptosis.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Antifolate resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Endocrine and metabolic diseases > Type I diabetes mellitus.

· Human Diseases > Neurodegenerative diseases > Alzheimer's disease.

· Human Diseases > Neurodegenerative diseases > Prion diseases.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > African trypanosomiasis.

· Human Diseases > Infectious diseases: Parasitic > Malaria.

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Measles.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Human Diseases > Immune diseases > Graft-versus-host disease.

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Cytosolic DNA-sensing pathway.   (View pathway)

· Organismal Systems > Immune system > Hematopoietic cell lineage.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Sensory system > Inflammatory mediator regulation of TRP channels.   (View pathway)


1). Wu C et al. Betulinic Acid Inhibits ROS-Mediated Pyroptosis in Spinal Cord Injury by Augmenting Autophagy via the AMPK-mTOR-TFEB Signaling Pathway. Int J Biol Sci 2021 Mar 11;17(4):1138-1152. (PubMed: 33867836) [IF=10.750]

Application: WB    Species: Mice    Sample: spinal cords

Figure 2 BA attenuates pyroptosis after SCI. (A) Immunofluorescence staining for Caspase-1 and NeuN co-localization in the spinal cords of the Sham, SCI, and BA groups (scale bar = 25 µm) (B) The quantitative mean optical density of the Caspase-1 in motor neurons of spinal cord lesion. (C) Immunofluorescence staining for GSDMD and NeuN co-localization in the spinal cords of the Sham, SCI, and BA groups (scale bar = 25 µm) (D) The quantitative mean optical density of the GSDMD in motor neurons of spinal cord lesion. (E)Western blotting for ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels in the Sham, SCI, and BA groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (F) The optical density values of the ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels were quantified and analyzed in each group. The values are expressed as the means ± SEM, n=5 per group. **p< 0.01, vs. Sham group. #p< 0.05 and ##p< 0.01, vs. SCI group.

2). Ding T et al. An in situ tissue engineering scaffold with growth factors combining angiogenesis and osteoimmunomodulatory functions for advanced periodontal bone regeneration. J Nanobiotechnology 2021 Aug 17;19(1):247. (PubMed: 34404409) [IF=10.435]

3). Liu W et al. Micheliolide Ameliorates Diabetic Kidney Disease by Inhibiting Mtdh-mediated Renal Inflammation in Type 2 Diabetic db/db Mice. Pharmacol Res 2019 Oct 24:104506 (PubMed: 31669149) [IF=10.334]

4). Wang Z et al. TRPV4-induced inflammatory response is involved in neuronal death in pilocarpine model of temporal lobe epilepsy in mice. Cell Death Dis 2019 May 16;10(6):386 (PubMed: 31097691) [IF=9.685]

Application: WB    Species: mouse    Sample: NRLP3 inflammasome

Fig. 2| TRPV4 agonist increases NRLP3 inflammasome expression and proinflammatory cytokine production. a–c The hippocampal protein levels of NLRP3 (a), ASC (b) and caspase-1 (c) in control and GSK1016790A-injected mice. **P < 0.01 vs. control. d–f Icv. of TRPV4 agonist GSK1016790A markedly increased the protein levels of IL-1β (d), TNF-α (e) and IL-6 (f) in hippocampi.

5). Dai X et al. A non‐retinol RAR‐γ selective agonist‐tectorigenin can effectively inhibit the UVA‐induced skin damage. Br J Pharmacol 2022 Jun 22. (PubMed: 35731978) [IF=9.473]

6). Mei J et al. Shufengjiedu capsules protect against neuronal loss in olfactory epithelium and lung injury by enhancing autophagy in rats with allergic rhinitis. Biosci Trends 2020 Jan 20;13(6):530-538 (PubMed: 31866616) [IF=9.083]

Application: WB    Species: Rat    Sample: lung tissues

Figure 3. SFJDCs reduced increased TNF-α and IL-1β levels in serum, the lungs, and OE. (A): Bar graph of TNF-α and IL-1β concentrations in serum detecting with ELISA. (B): Western blot bands of TNF-α and IL-1β protein in lung tissue. Bar graph of levels of TNF-α and IL-1β protein in lung tissue. (C): Immunohistochemistry staining of TNF-α in OE tissue. (D): Immunofluorescent staining of IL-1β in OE tissue. Data are representative of at least three separate experiments. (*p < 0.05, **p < 0.01 vs. control group; # p < 0.05, ##p < 0.01, ###p < 0.001 vs. model group).

7). Tao HC et al. CD47 Deficiency in Mice Exacerbates Chronic Fatty Diet-Induced Steatohepatitis Through Its Role in Regulating Hepatic Inflammation and Lipid Metabolism. Front Immunol 2020 Feb 25;11:148 (PubMed: 32158445) [IF=8.786]

8). Xia C et al. Autophagy and Exosome Coordinately Enhance Macrophage M1 Polarization and Recruitment in Influenza A Virus Infection. Front Immunol 2022 Mar 17;13:722053. (PubMed: 35371077) [IF=8.786]

Application: WB    Species: mouse    Sample: macrophages

FIGURE s4 |The total proteins of infected primary peritoneal macrophages were extracted at 24, 36, 48, and 72 h post-infection and then subjected for Western blotting. The corresponding antibodies were used to analyze autophagic protein (LC3, p62), exosome marker (CD63), and IL-1β activation pathway (IL-1β, cleaved IL-1β, and caspase-1) normalized to GAPDH.

9). Liu X et al. Combination of resolvin E1 and lipoxin A4 promotes the resolution of pulpitis by inhibiting NF-κB activation through upregulating sirtuin 7 in dental pulp fibroblasts. Cell Prolif 2022 Apr 11;e13227. (PubMed: 35411569) [IF=8.755]

Application: WB    Species: rat    Sample: Dental pulp fibroblasts

FIGURE 1 |Effects of combined administration of RvE1 and LXA4 on pro-inflammatory factor expression.(C) NLRP3, (D) caspase-1, (E) IL-1β and (F) IL-18 mRNA levels on LPS-induced DPFs detected by qPCR and (G) their protein levels tested by western blotting (normalized to that of β-tubulin).

10). She P et al. Dextran sulfate-triamcinolone acetonide conjugate nanoparticles for targeted treatment of osteoarthritis. Int J Biol Macromol 2020 May 7 (PubMed: 32389649) [IF=8.025]

Application: IHC    Species: Mouse    Sample: RAW 264.7 cells

Fig. 6. (A) Efficacies of NS, TA, DS and DS-TA NPs in treating OA, as shown by articular sections stained with H&E or safranin O, and their corresponding immunohistochemical staining sections. Scale bar: 100 μm. (B, C, D) The levels of IL-1β, IL-6 and TNF-α in cartilage samples in each treatment group. Date are presented as mean ± SD (n = 3, *p b 0.05).

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