LILRB1 Antibody (YA4377)(PBS only)
(Synonyms: ILT2; LIR1; MIR7; PIRB; CD85J; ILT-2; LIR-1; MIR-7; PIR-B)LILRB1 Antibody (YA4377) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to LILRB1.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, ELISA
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Reactivity :
Human
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Formulation:
Supplied in PBS, pH 7.4.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|
| Dilution Ratio | 1:500-1:2000 | 1:10000 |
Product Details
LILRB1 Antibody (YA4377) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to LILRB1.
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Host Mouse
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Species ReactivityHuman
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Observed Molecular WeightObserved band size: 110 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 71 kDa
Purified recombinant fragment of human LILRB1 (AA: extra 338-461) expressed in E. Coli.
affinity purified.
Non-conjugated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS, pH 7.4.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
Leukocyte immunoglobulin-like receptor B1 (LILRB1) functions as an inhibitory immune checkpoint that modulates neutrophil activation and migration[1]. Mechanistically, LILRB1 attenuates neutrophil extracellular trap (NET) formation by suppressing pro-inflammatory cytokine release, including IL-1β, IL-6, and IL-8, in drug-resistant Pseudomonas aeruginosa-associated bronchiectasis[1]. This receptor operates through interactions with soluble HLA-G, with inverse correlations observed between LILRB1 expression and disease severity indices or peripheral neutrophil counts[1]. Compared with related inhibitory receptors, LILRB1 uniquely regulates neutrophil migration in co-culture models, reducing chemotactic responses toward infected bronchial epithelial cells[1]. Experimental applications of recombinant LILRB1 protein demonstrate suppression of NETosis and inflammatory cytokine production, highlighting its potential as a modulatory agent in neutrophil-driven airway inflammation[1]. In addition, LILRB1 signaling may converge with PI3K/Akt/mTOR pathways, consistent with inhibitory roles observed in axonal outgrowth and immune cell regulation, although direct mechanistic links remain under investigation[2]. Collectively, LILRB1 serves as a critical checkpoint in neutrophil-mediated inflammation, providing a framework for studying immunomodulatory interventions and selective agonist or inhibitory strategies in respiratory disease models[1][2].
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Subcellular Localization
Cell membrane; Single-pass type I membrane protein; Secreted
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Expression
Tissue_specificity:Expression (protein level) in B cells, monocytes, and various dendritic cell (DC) subsets (including myeloid, plasmacytoid, and tolerant DCs) (PubMed:20448110, PubMed:24453251, PubMed:9285411, PubMed:9842885) . Expression (protein level) in decidual macrophages (PubMed:19304799) . Expression (protein level) in decidual NK cells (PubMed:29262349) . -
Isoforms & Post-Translational Modification
Q8NHL6 has 5 isomers: Q8NHL6-1: 70819 Da (predicted); Q8NHL6-2: 70890 Da (predicted); Q8NHL6-3: 71019 Da (predicted); Q8NHL6-4: 70948 Da (predicted); Q8NHL6-5: 49356 Da (predicted).
Phosphorylated on tyrosine residues. Dephosphorylated by PTPN6 -
Subunit
Binds PTPN6 when phosphorylated (PubMed:9285411). Binds FCER1A and FCGR1A (PubMed:11907092, PubMed:9842885). Interacts with human cytomegalovirus/HHV-5 protein UL18 (PubMed:10591185). Interacts with peptide-bound HLA-G-B2M complex (PubMed:16455647). Interacts with peptide-bound HLA-F-B2M complex but not with peptide-free HLA-F open conformer. It does not probe the peptide sequence directly (PubMed:28636952)
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SwissProt ID
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Synonyms
ILT2; LIR1; MIR7; PIRB; CD85J; ILT-2; LIR-1; MIR-7; PIR-B
Documentation
References
[1]. Bi YY, et al. PirB inhibits axonal outgrowth via the PI3K/Akt/mTOR signaling pathway. Mol Med Rep. 2018 Jan;17(1):1093-1098. [Content Brief]
[2]. Zheng S, et al. LILRB1 Modulates Neutrophil Migration, NETosis, and Inflammation in Drug-Resistant Pseudomonas aeruginosa-Associated Bronchiectasis. Infect Drug Resist. 2026 Feb 23;19:581113. [Content Brief]
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