Mouse IL-28A/IFN-lambda 2 Antibody Summary
Asp20-Val193
Accession # NP_001019844
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Scientific Data
IL‑28A/IFN‑ lambda 2 Inhibition of EMCV-induced Cytopathy and Neutralization by Mouse IL‑28A/IFN‑ lambda 2 Antibody. Recombinant Mouse IL-28A (Catalog # 4635-ML) reduces the Encephalomyocarditis Virus (EMCV)-induced cytopathy in the HepG2 human hepatocellular carcinoma cell line in a dose-dependent manner (orange line). Inhibition of EMCV activity elicited by Recombinant Mouse IL-28A (20 ng/mL) is neutralized (green line) by increasing concentrations of Sheep Anti-Mouse IL-28A Antigen Affinity-purified Polyclonal Antibody (Catalog # AF4635). The ND50 is typically 3-15 µg/mL.
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: IL-28A/IFN-lambda 2
IL-28A (also named interferon-lambda 2, IFN-lambda 2), IL-28B (IFN-lambda 3) and IL-29 (IFN-lambda 1) are type III interferons that are class II cytokine receptor ligands (1‑4). They are distantly related to members of the IL-10 family and type I IFN family (1‑4). Mouse IL-28A cDNA encodes a 193 amino acid (aa) protein with a 19 aa signal peptide and a 174 aa mature protein that lacks N-glycosylation sites. Mature mouse IL-28A shares 81% and 66% aa sequence identity with rat and human IL-28A, respectively, and functions across species (5). Mouse IL-28A and IL-28B share 97% aa identity; the mouse lacks a functional IL-29 gene (4). Type III interferons are widely expressed, but are mainly produced by antigen presenting cells in response to viruses and double-stranded RNA that interact with Toll-like receptors or RIG-1 family helicases (2‑6). They signal through a widely expressed receptor that is a heterodimer of the IL-10 receptor beta (IL-10 R beta ) and IL-28 receptor alpha (IL-28 R alpha ; also called IFN-lambda R1) (2, 3, 7, 9). Interaction of either type I or type III IFNs with their receptors activates similar pathways, including JAK tyrosine kinase activation, STAT phosphorylation and formation of the IFN-stimulated regulatory factor 3 (ISGF-3) transcription factor complex (1‑3). Both type I and III IFNs induce antiviral activity and upregulate MHC class I antigen expression (2‑6). Cell lines responsive to type III IFNs are also responsive to type I IFNs, but in general, higher concentrations of type III IFNs are needed for similar in vitro responses (8). In vivo, however, type III IFNs enhance levels of IFN-gamma in serum, suggesting that the robust antiviral activity of type III IFNs may stem in part from activation of the immune system (5, 7). Anti-proliferative and antitumor activity in vivo has also been shown for type III IFNs (9‑11).
- Chen, Q. et al. (2006) Vitam. Horm. 74:207.
- Sheppard, P. et al. (2003) Nat. Immunol. 4:63.
- Kotenko, S.V. et al. (2003) Nat. Immunol. 4:69.
- Bartlett, N.W. et al. (2005) J. Gen. Virol. 86:1589.
- Ank, N. et al. (2006) J. Virol. 80:4501.
- Onoguchi, K. et al. (2007) J. Biol. Chem. 282:7576.
- Siebler, J. et al. (2007) Gastroenterology 132:358.
- Meager, A. et al. (2005) Cytokine 31:109.
- Lasfar, A. et al. (2006) Cancer Res. 66:4468.
- Sato, A. et al. (2006) J. Immunol. 176:7686.
- Zitzmann, K. et al. (2006) Biochem. Biophys. Res. Commun. 344:1334.
Product Datasheets
Citation for Mouse IL-28A/IFN-lambda 2 Antibody
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.
1 Citation: Showing 1 - 1
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Regulation of Th17/Treg Balance by 27-Hydroxycholesterol and 24S-Hydroxycholesterol Correlates with Learning and Memory Ability in Mice
Authors: Tao Wang, Shanshan Cui, Ling Hao, Wen Liu, Lijing Wang, Mengwei Ju et al.
International Journal of Molecular Sciences
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