Enzo：CpG ODN，寡聚脫氧核苷酸家族產品

免疫佐劑，是一類可以增強抗原免疫原性的免疫調節分子、化合物或大分子復合物。大多數佐劑可以通過啟動先天免疫系統來輔助抗原應答。先天免疫系統通過模式識別受體（pattern recognition receptor，PRR）來感知各種微生物表達的病原體相關分子模式（PAMPs）的存在，激活對病原體的先天性免疫信號通路并調節適應性免疫應答。添加天然或人工合成的佐劑分子有助于恢復或改進純化抗原的免疫原性，調節免疫應答類型，在現代疫苗學研究中具有重要意義。含 CpG 序列的寡脫氧核苷酸（oligonucleotide，ODN）可模擬哺乳動物免疫系統的“危險信號”，參與機體免疫應答的調節，增強疫苗的免疫原性。

  艾美捷科技為您推薦Enzo Life Sciences精品低內毒素的CpG ODN，寡聚脫氧核苷酸全家族產品。

 * 更多CpG ODN，寡聚脫氧核苷酸產品，歡迎垂詢艾美捷。

* 上述產品，僅供科研使用，不得用于醫療. 

【CpG ODN，寡聚脫氧核苷酸全家族產品優勢】

1、無內毒素水，ddWater 

2、除對照產品外，產品內均已提供陰性對照 

3、無菌，凍干粉，內毒素<0.002EU/?g 

4、BULK：可用于體內實驗  

【Cell文章鑒賞】

IF=66.8, 《Systematic discovery of TLR signaling components delineates viral-sensing circuits 》,Cell

【Enzo精品低內毒素的CpG ODN，寡聚脫氧核苷酸，更多發表文章】

• Ban, T., Kikuchi, M., Sato, G.R. et al. Genetic and chemical inhibition of IRF5 suppresses pre-existing mouse lupus-like disease. Nat Commun12, 4379 (2021).

• Contact-dependent inhibition of HIV-1 replication in ex vivo human tonsil cultures by polymorphonuclear neutrophils: T. Reif, et al.; Cell Rep. Med. 2, 100317 (2021)

• Homeostatic and Pathogenic Roles of GM3 Ganglioside Molecular Species in TLR4 Signaling in Obesity: H. Kanoh, et al.; EMBO J. 39, e101732 (2020)

• Murakami, Yuki, et al. "Increased regulatory B cells are involved in immune evasion in patients with gastric cancer." Scientific reports 9.1 (2019): 1-9.

• Maatouk, L., Compagnion, AC., Sauvage, MA.Cd. et al. TLR9 activation via microglial glucocorticoid receptors contributes to degeneration of midbrain dopamine neurons. Nat Commun9, 2450 (2018).

• Okamura, T., Sumitomo, S., Morita, K. et al. TGF-β3-expressing CD4+CD25?LAG3+ regulatory T cells control humoral immune responses. Nat Commun6, 6329 (2015).

• Chevrier, Nicolas et al. "Systematic discovery of TLR signaling components delineates viral-sensing circuits". Cell vol .147,4 (2011): 853-67.

• Larson, S. R., et al. "Ly6C+ monocyte efferocytosis and cross-presentation of cell-associated antigens." Cell Death & Differentiation 23.6 (2016): 997-1003.

• Jia, Xianxian, et al. "CCK 8 negatively regulates the TLR 9‐induced activation of human peripheral blood p DC s by targeting TRAF 6 signaling." European Journal of Immunology 44.2 (2014): 489-499.

• TLR9-signaling is required for turning retinoic acid into a potent stimulator of RP105 (CD180)-mediated proliferation and IgG synthesis in human memory B cells: A. Eriksen, et al.; Cell. Immunol. 279, 87 (2012)

• Activation of murine macrophages via TLR2 and TLR4 is negatively regulated by a Lyn/PI3K module and promoted by SHIP1: S. Keck, et al.; J. Immunol. 184, 5809 (2010)

• Cutting edge: the mechanism of invariant NKT cell responses to viral danger signals: A.J. Tyznik, et al.; J. Immunol. 181, 4452 (2008)

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