免疫佐剂（immunoadjuvant）,又称非特异性免疫增生剂，其本身不具有抗原性，但同抗原一起或者预先注射到机体后，能非特异性地改变机体对该抗原的特异性免疫应答。1925年Ramon首先发现在疫苗中加入某种其他物质可以提高抗原的特异性免疫应答，后来此种物质被命名为免疫佐剂，随后各种各样的不同物质被用做免疫佐剂，从而大大提高了疫苗的保护性效力。免疫佐剂在增强疫苗的免疫作用中发挥了极大的功能，并且经历了从天然佐剂到人工佐剂的演变。
免疫佐剂目前有多种种类，可分为传统免疫佐剂、细胞因子免疫佐剂、天然来源免疫佐剂和新型免疫佐剂。
CpG-ODN作为免疫佐剂的应用：
CpG-ODN能协同抗原刺激特异性B细胞和T细胞的分化，可作为高效的疫苗佐剂。CpG-DNA能同时增强体液免疫应答和细胞免疫应答,尤其对细胞免疫应答具有更突出的增强作用。CpG-ODN几乎对所有蛋白质抗原和灭活疫苗具有佐剂作用,而且在与其它佐剂合用时还可弥补其他佐剂诱导Th2型免疫应答的缺陷。
CpG-DNA安全有效的佐剂特性，使其成为佐剂领域的研究热点，特别是能使灭活疫苗及可溶性蛋白抗原等诱导的Th2反应向Th1反应转换，增加对疾病的保护性。
CpG-ODN可作为免疫治疗药物
CpG序列在动物体内能激发强烈的Th1相关的免疫反应，抑制Th2相关免疫反应。利用这些特点，有可能用CpG-DNA治疗过敏反应如哮喘及Th2相关的自体免疫疾病。
艾美捷CpG-ODN寡聚脱氧核苷酸特点：
1、无内毒素水，ddWater
2、除对照产品外，产品内均已提供阴性对照
3、无菌，冻干粉，内毒素<0.002EU/?g
4、BULK：可用于体内实验
艾美捷CpG ODN Cell文章鉴赏：
IF=66.8, 《Systematic discovery of TLR signaling components delineates viral-sensing circuits 》,Cell
艾美捷CpG ODN 更多发表文章：
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)
