免疫佐劑（immunoadjuvant）,又稱非特異性免疫增生劑，其本身不具有抗原性，但同抗原一起或者預先注射到機體后，能非特異性地改變機體對該抗原的特異性免疫應答。1925年Ramon首先發(fā)現在疫苗中加入某種其他物質可以提高抗原的特異性免疫應答，后來此種物質被命名為免疫佐劑，隨后各種各樣的不同物質被用做免疫佐劑，從而大大提高了疫苗的保護性效力。免疫佐劑在增強疫苗的免疫作用中發(fā)揮了極大的功能，并且經歷了從天然佐劑到人工佐劑的演變。

免疫佐劑目前有多種種類，可分為傳統(tǒng)免疫佐劑、細胞因子免疫佐劑、天然來源免疫佐劑和新型免疫佐劑。

CpG-ODN作為免疫佐劑的應用：

CpG-ODN能協同抗原刺激特異性B細胞和T細胞的分化，可作為高效的疫苗佐劑。CpG-DNA能同時增強體液免疫應答和細胞免疫應答,尤其對細胞免疫應答具有更突出的增強作用。CpG-ODN幾乎對所有蛋白質抗原和滅活疫苗具有佐劑作用,而且在與其它佐劑合用時還可彌補其他佐劑誘導Th2型免疫應答的缺陷。

CpG-DNA安全有效的佐劑特性，使其成為佐劑領域的研究熱點，特別是能使滅活疫苗及可溶性蛋白抗原等誘導的Th2反應向Th1反應轉換，增加對疾病的保護性。

CpG-ODN可作為免疫治療藥物

CpG序列在動物體內能激發(fā)強烈的Th1相關的免疫反應，抑制Th2相關免疫反應。利用這些特點，有可能用CpG-DNA治療過敏反應如哮喘及Th2相關的自體免疫疾病。

艾美捷CpG ODN 寡聚脫氧核苷酸特點：

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  

艾美捷CpG ODN Cell文章鑒賞：

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

艾美捷CpG ODN 更多發(fā)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)