Ifnl3-KO Mouse
一般名
Ifnl3-KO
製品ID
S-KO-18327
背景情報
C57BL/6JCya
系統ID
KOCMP-338374-Ifnl3-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Ifnl3-KO Mouse（カタログ番号S-KO-18327）はサイアジェンから購入しました。」と引用してください。
製品タイプ
年齢
遺伝子型
性別
数量
標準的な配送方法では、少なくとも3匹のヘテロ接合体キャリアを保証しています。ホモ接合体キャリアや指定された性別の個体の繁殖サービスも利用可能です。
基本情報
系統名
Ifnl3-KO
系統ID
KOCMP-338374-Ifnl3-B6J-VA
遺伝子名
製品ID
S-KO-18327
遺伝子別名
Il28, IFL-1, Il28b, IL-28B, If1ia2, INF-alpha, INF-lambda
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conventional knockout
染色体
Chr 7
表現型
アプリケーション
--
さらに
系統詳細
EnsemblトランスクリプトID
ENSMUST00000078364
NCBIトランスクリプトID
NM_177396
ターゲット領域
Exon 1~5
有効領域の大きさ
~3.4 kb
遺伝子研究の概要
Ifnl3, also known as IL28B, is a gene that encodes a protein belonging to the interferon lambda family. Interferons play crucial roles in the innate immune response, regulating the body's defense against viral infections and modulating immune cell functions. The pathways associated with Ifnl3 are related to antiviral responses and immune regulation, which are of great biological importance in maintaining the body's health [2,4,5,6]. Genetic models can be valuable in studying Ifnl3 to understand its precise functions and implications in disease.
In relation to diseases, Ifnl3 polymorphisms have been extensively studied. In COVID-19 patients, carriers of at least one variant allele of Ifnl3 rs8099917 were almost 36-fold more likely not to survive SARS-CoV-2 infection, indicating that this polymorphism significantly affects the outcome of COVID-19 [1]. For chronic hepatitis B (CHB) patients, two polymorphisms (rs12979860 and rs8099917) of Ifnl3 may play a crucial role in interferon-based treatment, especially in the HBeAg-positive group [2]. In systemic sclerosis, the Ifnl3 polymorphism is associated with pulmonary fibrosis, and serum IFN-λ3 levels are higher among subjects with pulmonary fibrosis [3]. Regarding hepatitis C virus (HCV) infections, Ifnl3 SNPs are the strongest baseline predictors of sustained virologic response to pegylated interferon and ribavirin therapy in HCV genotype 1, 2, or 3 infections [4,7]. An Ifnl3-adjuvanted HCV DNA vaccine can reduce regulatory T cell frequency and increase virus-specific T cell responses, showing potential in preventing HCV re-infection [8].
In conclusion, Ifnl3 is a key gene in the innate immune response, playing a significant role in various viral-related diseases such as COVID-19, hepatitis B, and hepatitis C, as well as in fibrotic conditions like pulmonary fibrosis in systemic sclerosis. Studies on Ifnl3, especially those involving its polymorphisms, help in understanding disease mechanisms and can potentially guide therapeutic decision-making for these diseases.
References：
1. Matic, Sanja, Milovanovic, Dragan, Mijailovic, Zeljko, Baskic, Dejan, Djordjevic, Natasa. . IFNL3/4 polymorphisms as a two-edged sword: An association with COVID-19 outcome. In Journal of medical virology, 95, e28506. doi:10.1002/jmv.28506. https://pubmed.ncbi.nlm.nih.gov/36655749/
2. Zhao, Zhongyi, Qin, Zhen, Zhou, Linlin, Wang, Baoning, Li, Mingyuan. 2019. The impact of IFNL3 genotype on interferon treatment outcome in patients chronically infected with hepatitis B virus: A meta-analysis. In Microbial pathogenesis, 134, 103598. doi:10.1016/j.micpath.2019.103598. https://pubmed.ncbi.nlm.nih.gov/31201901/
3. Metwally, Mayada, Thabet, Khaled, Bayoumi, Ali, George, Jacob, Eslam, Mohammed. 2019. IFNL3 genotype is associated with pulmonary fibrosis in patients with systemic sclerosis. In Scientific reports, 9, 14834. doi:10.1038/s41598-019-50709-9. https://pubmed.ncbi.nlm.nih.gov/31619697/
4. Chinnaswamy, Sreedhar. 2014. Genetic variants at the IFNL3 locus and their association with hepatitis C virus infections reveal novel insights into host-virus interactions. In Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 34, 479-97. doi:10.1089/jir.2013.0113. https://pubmed.ncbi.nlm.nih.gov/24555572/
5. O'Connor, Kate S, Ahlenstiel, Golo, Suppiah, Vijayaprakash, George, Jacob, Booth, David R. 2013. IFNL3 mediates interaction between innate immune cells: Implications for hepatitis C virus pathogenesis. In Innate immunity, 20, 598-605. doi:10.1177/1753425913503385. https://pubmed.ncbi.nlm.nih.gov/24045339/
6. O'Connor, Kate S, George, Jacob, Booth, David, Ahlenstiel, Golo. . Dendritic cells in hepatitis C virus infection: key players in the IFNL3-genotype response. In World journal of gastroenterology, 20, 17830-8. doi:10.3748/wjg.v20.i47.17830. https://pubmed.ncbi.nlm.nih.gov/25548481/
7. Eslam, Mohammed, Leung, Reynold, Romero-Gomez, Manuel, George, Jacob, Ahlenstiel, Golo. 2014. IFNL3 polymorphisms predict response to therapy in chronic hepatitis C genotype 2/3 infection. In Journal of hepatology, 61, 235-41. doi:10.1016/j.jhep.2014.03.039. https://pubmed.ncbi.nlm.nih.gov/24768758/
8. Han, Ji Won, Sung, Pil Soo, Hong, Seon-Hui, Ahn, Sang Hoon, Shin, Eui-Cheol. 2020. IFNL3-adjuvanted HCV DNA vaccine reduces regulatory T cell frequency and increases virus-specific T cell responses. In Journal of hepatology, 73, 72-83. doi:10.1016/j.jhep.2020.02.009. https://pubmed.ncbi.nlm.nih.gov/32088322/
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