The preparation of blocking or antagonistic antibodies to CD40 can not only be used to detect the expression of CD40, but also to the treatment of inflammatory diseases or tumor immunotherapy. By using a recombinant CD40 protein, we generated fourteen hybridoma cell lines to produce CD40 antibodies. All the CD40 monoclonal antibodies could be used to detect the CD40 expression via western blotting, nine of which can also be used for FACS and one CD40 monoclonal antibody can block the CD40-CD40L interaction. Importantly, we got eight clones that produced agonistic antibodies to human CD40, while ten of the clones could activate the CD40 downstream gene expression of mouse splenocytes and seven of the clones could upregulate the expression of CD86 on mice B cells. Therefore, the CD40 monoclonal antibodies we generated can be used to test the expression of CD40, and to block or activate the CD40 signal.

Interferon regulatory factor 4 (IRF4) is an evolutionarily conserved regulatory molecule that is expressed in varying levels at key stages of differentiation of many immune cells. In terms of its role in the differentiation of innate immune cell lineages, IRF4 is one of the key transcription factors regulating M2-like macrophage polarization and differentiation of both monocyte-derived DC and conventional DC 2 (cDC2). On the other hand, on the differentiation and fate determination of adaptive immune cell subgroups, IRF4 plays a broad role and controls all levels of differentiation of these immune cell subgroups in that IRF4 regulates the differentiation of the naive CD4⁺ T cells into various subsets (Th1, Th2, Th9, Th17, Treg, and follicular helper T cell ［Tfh］). In addition, it also dictates the differentiation of naive CD8⁺ T cells into effector cells. At the same time, IRF4 also regulates B cell differentiation cycle and plasma cell function, thereby affecting humoral immunity. The recent progress in the study of IRF4's involvement in the regulation of immune cell lineage differentiation and fate determination is summarized in this review.

代谢和免疫是机体生存最基本的需求。在长期的进化过程中，各种生物都形成了代谢和免疫反应的共同通路。因此，免疫反应和代谢调节高度统一，功能上相互依赖，这种免疫和代谢之间的相互作用可以被看作机体稳态调节的核心机制。代谢免疫学就在代谢和免疫相互联系的基础上研究免疫与代谢之间相互作用的途径、模式及其调控的一门新兴学科，并在此基础上更好地了解相关疾病的病理机制,探讨新的治疗方法。代谢免疫学的全新时代正在到来。

机体衰老过程中不仅免疫器官组织会发生相应的变化，免疫功能也会下降。T淋巴细胞是免疫系统的主要组成部分，不仅参与体液免疫，也参与细胞免疫。鉴于国内对T淋巴细胞增龄性变化研究较少，本文主要综述小鼠衰老过程中，不同月龄小鼠T淋巴细胞亚群的数量和功能的变化。整理发现，小鼠成年之后，CD4⁺T淋巴细胞在胸腺、外周血和脾脏中均发生增龄性的减少，CD8⁺T细胞则仅在胸腺中发生增龄性的减少，而在外周血和脾脏中发生增龄性的增加，但两者都会出现一定的功能障碍，其中包括增殖能力和免疫功能。

糖基化修饰对单克隆抗体的结构、功能及药代动力学会产生影响。不同糖型结构通过与FcRs、Clq以及新生Fc受体(neonatal Fc receptor， FcRn)的结合而分别调节抗体依赖的细胞介导的细胞毒作用(antibody-dependent cytotoxicity， ADCC)、补体依赖的细胞毒作用(complement-dependent cytotoxicity， CDC)以及FcRn介导的药物消除半衰期。不同的细胞表达系统和细胞培养条件均会对糖基化的类型及程度产生影响，进而影响治疗性抗体的疗效以及安全性。通过糖基化工程可以控制特定糖型的形成，进一步优化单克隆抗体的效应功能和降低免疫原性。本文就单克隆抗体糖基化修饰研究进展进行综述。

T细胞作为主要的免疫细胞在肿瘤发展和治疗的各个阶段发挥重要作用，而T细胞与肿瘤细胞共培养是建立T细胞与肿瘤细胞之间相互作用模型的重要途径。但是，有关T细胞与肿瘤细胞共培养方法存在一定难度并缺乏统一性，导致相关研究和应用发展缓慢。该综述主要概述并总结CD4⁺和CD8⁺T细胞与肿瘤细胞共培养的方法和应用。

自噬是真核生物对细胞应激物如错误折叠蛋白、长寿蛋白、受损的细胞器或胞内抗原进行降解的一种代谢途径。自噬与多种疾病相关，如神经退行性疾病、癌症等。现在发现，自噬与自身炎症性疾病（autoinflammatory disease， AUID）也存在较大关联。AUID是一类由遗传异质性因素引起的疾病，偶发性炎症、先天免疫反应失调等均会引起或加剧该类疾病的发生。已有研究表明，自噬通过对先天免疫信号传导途径的调控，可以对炎症水平进行控制。AUID相关的遗传变体可以直接激活炎症信号通路，而这些变体也可能造成自噬功能损伤，从而间接增加炎症反应水平。AUID中的遗传变体可以通过不同的机制对自噬造成损伤，文章就几种AUID中相关变体对自噬影响的反应途径及作用机制进行综述，以期为自噬作为治疗AUID的靶点提供新的策略。

巨噬细胞，作为机体的专职高效吞噬细胞，在凋亡细胞的清除方面起着非常重要的作用，进而对凋亡细胞诱导的免疫反应也产生了举足轻重的影响。机体产生的自身抗原由巨噬细胞吞噬后向抗原特异性T细胞的提呈在免疫应答或维持自身免疫耐受中起着至关重要的作用。相反，凋亡细胞的吞噬通路异常则有可能导致系统性或器官特异性自身免疫性疾病的发生。本文综述了巨噬细胞吞噬凋亡细胞之后对机体免疫调节的影响，特别是凋亡细胞被吞噬之后在自身免疫性疾病与免疫耐受方面的影响。

 Neutrophils are one of the most important effector cells in innate immunity and the defense at the frontline against invading pathogens. With the continuous advances, people have realized that neutrophils not only participate in the inflammatory response and tissue damage repair, tumor-associated neutrophils also act as anti- or pro-tumorigenic factors depending on specific tumor microenvironment (TME) status. Neutrophils with different functions may have different phenotypes and also some plasticity. This review begins with the biological properties of neutrophils, and then summarizes the diverse phenotypes of neutrophils with different functions in the TME, the possible mechanisms of immunosuppressive neutrophils regulating tumor immunity, and the clinical application of neutrophils in cancer research.

肿瘤细胞独特的有氧糖酵解代谢为其增殖生长提供能量，消耗了肿瘤微环境中的大量营养。肿瘤微环境中也存在大量的免疫细胞，免疫细胞活化、执行效应功能会发生与肿瘤细胞类似的代谢重编程现象，亦需要大量能量。因此免疫细胞与肿瘤细胞之间会存在激烈的代谢竞争，同时也存在密切的代谢调控。通过调整肿瘤代谢和免疫代谢的平衡，人为地抑制肿瘤代谢、增强免疫代谢，提高肿瘤内的免疫功能可能为肿瘤免疫治疗开辟一个新的方向。

More and more studies have shown that the occurrence of atherosclerosis is closely related to pyroptosis, especially gasdermin D（GSDMD）-mediated pyroptosis. In atherosclerosis, inflammatory cells such as macrophages, vascular endothelial cells, and vascular smooth muscle cells undergo pyroptosis, leading to plaque rupture and thrombosis, and finally to acute coronary syndrome. In the development of atherosclerosis, arterial wall endothelial injury and lipid deposition are the main initiating factors, which activate Caspase-1 and Caspase-11/4/5, respectively, and in turn cause the cleavage of the GSDMD protein and mediate classical and non-classical cell pyroptosis. The N-terminus of the GSDMD protein migrates to the cell membrane and oligomerizes to form pores through which the inflammatory factors IL-1β and IL-18 are released into the interstitium. The release of inflammatory factors further promotes the death of intravascular cells, after which their contents, cytokines, and proteases enter the extracellular matrix, aggravating the local inflammatory response, leading to atherosclerotic plaque rupture and cardiovascular disease. Based on the above mechanism, the development of drugs that directly target GSDMD and signal molecules in the pyroptosis signaling pathway induced by GSDMD, such as inflammasomes, Caspase-1, IL-1β, and IL-18, provides a theoretical basis and new ideas for the treatment of atherosclerosis.

To compare the transfection efficiency of cationic liposome lipofectamine3000 (Lipo3000) in different cell types, miRNA mimics with different concentrations were transfected into NIH3T3, EL4and CD4⁺T cells respectively by Lipo3000. The differences in transfection efficiency were compared by FACS among different types of cells and among different concentrations of miRNA mimics groups in the same types of cells. The results indicated that the highest transfection efficiency in NIH3T3 would be obtained when transfected with 100 nmol/L miRNA mimics by Lipo3000. For EL4 and CD4⁺T cells, the efficiency of transfection was improved with the increase of miRNA mimics concentration and could reach up to (12.13 ± 1.16)% and (3.80 ± 0.60%) respectively. It could be concluded that the transfection efficiency of Lipofectamine 3000 for adherent cells and suspension cells was significantly higher than that in primary cells.

免疫细胞代谢机制研究是免疫代谢研究的一个重要方向。免疫细胞在增殖、分化以及效应功能的执行等过程中会发生代谢重编程现象。本文综述了不同类型的免疫细胞静息或激活状态下的代谢通路。

TIL是从肿瘤组织中分离出的浸润性淋巴细胞。1986年Rosenberg研究组首先报道了在黑色素瘤患者的肿瘤组织中存在渗入性的淋巴细胞——TIL，这些细胞从瘤体中分离并经IL-2激活后可大量扩增，并对自身肿瘤有高度特异性杀伤活性。一般来说，TIL中绝大多数细胞是CD3⁺T细胞，不同肿瘤来源的TIL中，CD4⁺T细胞、CD8⁺T细胞的比例也有所差异，但大多数情况下以CD8⁺T细胞为主，其属于肿瘤过继免疫治疗中的高效效应细胞，其抗瘤效力相比LAK细胞强50～100倍。近年来，TIL的生物学表型及功能研究有了较大发展，这为TIL的临床应用带来了有利的价值，但目前国内外依然没有统一的培养技术规范。因此文章就目前TIL的研究进展以及各大实验室关于TIL的培养技术经验做一简要总结，以帮助基础科研及临床转化有效顺利地进行。

T细胞免疫球蛋白黏蛋白分子3（T cell immunoglobulin and mucin domain containing molecule 3，Tim-3）是T细胞免疫球蛋白黏蛋白家族的重要成员，最初在活化的Th1和CTL上被鉴定出来，并与其配体半乳糖凝集素9(galectin 9，Gal-9)结合后诱导T细胞死亡或衰竭。随着近年来对Tim-3的研究越来越多，发现Tim-3与其他配体，如磷脂酰丝氨酸（phosphatidylserine，PS）、高迁移率族蛋白B-1（high-mobility group box-1 protein， HMGB1）、CEA相关细胞黏附分子1（CEA-related cellular adhesion molecule 1，CEACAM-1）等结合，表现出不同的生物学作用，且Tim-3的表达在多种疾病中有不同程度的变化。研究者尝试以此作为免疫干预的靶点，并取得了一定的成果。文章通过对Tim-3及Tim-3在炎症性疾病、变态反应性疾病以及肿瘤中的研究作一综述，以探讨Tim-3在疾病中的表达变化及作用机制，并对未来相关研究进行展望。

NK细胞作为固有免疫细胞，它的激活无MHC限制也不需预先致敏，其在肿瘤免疫治疗中的作用受到越来越多的关注。然而，在肿瘤发生过程中，肿瘤细胞依然可以逃避NK细胞的杀伤，相关机制也各有报道。为了解决此问题，近年来，在增强NK细胞抗肿瘤活性和提高NK细胞特异性杀伤肿瘤方面取得了令人瞩目的研究成果。这提示NK细胞在肿瘤免疫治疗中具有广阔的应用前景。本文主要对抗体介导的NK细胞、与受者杀伤细胞KIR不匹配的同种异体NK细胞、嵌合抗原受体介导的NK细胞和免疫检查点抑制剂联合NK细胞对肿瘤细胞的细胞毒活性进行归纳与总结，以期为后续肿瘤免疫治疗相关基础和临床应用研究提供较为清晰的思路和参考。

巨噬细胞是人体抵抗病原的第一道防线，在人体的免疫系统中发挥着重要作用，其在机体的新陈代谢、生长发育、组织修复以及稳态的维持等过程中也同样扮演着不可替代的角色，因此，巨噬细胞在靶向治疗多种疾病方面存在巨大潜力。同时，随着实验研究技术的不断发展，人类对于巨噬细胞的认识也得以发展，而这些研究成果将为巨噬细胞作为最具潜力的临床靶标的提供有效理论依据。故，对近年来不同组织定居巨噬细胞的起源和特异性发展，以及其在机体稳态和疾病时自我更新机制的研究进展，进行简单概述，将帮助我们全面了解巨噬细胞的功能特征，这对研究其在新陈代谢疾病、免疫疾病、组织修复、肿瘤及炎症等多种疾病的防治中作为治疗靶点具有重要意义，对人类抵抗疾病具有重大意义。

表达在APC表面的B7家族配体和T细胞表面的CD28家族受体是一对极为重要的共刺激分子。B7分子与CD28分子结合，作为第二信号调节T细胞的活性。以这2个家族分子作为靶点的肿瘤免疫治疗药物已经上市。糖基化是重要的蛋白质翻译后修饰方式，在细胞生长、发育、分化的各个阶段以及肿瘤的发生、发展过程中，对细胞和蛋白质功能的调节发挥着重要作用。文章对B7/CD28家族分子的糖基化研究进展情况进行综述。

NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome is a protein complex that stimulates the activation of caspase and the maturation of IL-1β, and promotes the pathogenesis and development of various inflammations. The occurrence of periodontitis (PD) is related to the dysbacteriosis of periodontal tissue. NLRP3 inflammasomes are involved in the activation of neutrophil, macrophage, osteoclast (OC), and human periodontal ligament fibroblast (HPLF). This review summarizes the effects of NLRP3 inflammasome in the related immune and stromal cells on PD, and outlines new ideas for PD treatment targeting NLRP3 inflammasome.

近年来，无菌小鼠在研究肠道菌群与成人大脑结构及行为异常的相关疾病、对2型糖尿病发病的影响、对疟原虫感染的调控等研究中做出了重要贡献。无菌小鼠独特的无菌状态，为人类在探究生命体生理、病理反应时去除了其余的影响因素，是一个非常有价值的研究工具。无菌小鼠由于自身免疫系统发育的迟缓导致相应的免疫器官、免疫细胞的功能和数量明显异于正常小鼠，故本文将对无菌小鼠的免疫系统研究进展作进一步的概述。

白细胞介素36(interleukin 36, IL-36)是IL-1家族新成员，由3个生物学功能相似的成员IL-36α、IL-36β和IL-36γ组成。IL-36成员的共同受体为IL-36R，可与IL-1受体辅助蛋白(IL-36RAcP)相结合形成二聚体。IL-36Ra是IL-36的天然拮抗剂。IL-36可以活化MAPK、NF-κB信号级联途径，影响和调控多种趋化因子、炎症介质和黏附分子的表达和释放，在疾病发生发展中具有重要作用。现就IL-36生物学特征、受体和受体拮抗剂及其与相关疾病的关系进行综述。

In order to figure out the pathogenesis of ankylosing spondylitis(AS) as well as the clinical significance of immunocytes in the development of the disease , we conducted this research to detect the difference of T cell subsets in peripheral blood of between AS patients and healthy controls, a group of 42 AS patients and a group of 42 healthy subjects (healthy control group)were enrolled. The immunocyte phenotypes were measured by flow cytometry, the cytokines were examined by ELISA, and the transcription factors were detected by Q-PCR. We found that there were significant differences in several subsets of T cells in the patients. Compared with the normal controls, the CD4⁺ subset took precedence in AS patients and the ratio of effector/naïve was especially higher. In particular, the percentages of Th1 and Tfh cell count were higher and the difference was of statistical significance. Meanwhile, the percentage of Treg was slightly higher. As to the cytokines, the concentration of IFN-γ and TGF-β were decreased remarkably while IL-21 was noticeably increased. With respect to the transcription factors, the ratio between BCL-6, RORγt, T-bet and Foxp3 were all increased. The above results show that the network of immune system in AS patients is of imbalance, and the related inflammatory immunemolecules are widely activated.

前列腺素(prostaglandin， PG)是花生四烯酸的小分子衍生物，在内分泌系统、心血管系统、生殖系统和神经系统中发挥多种生物学效应。PGE₂作为PG比较有代表性的一种亚型，是人体内重要的炎症介质，参与调节CD4⁺T细胞的分化及相关细胞因子的分泌，从而影响CD4⁺T细胞所介导的疾病的发生发展。本文就PGE₂及其对CD4⁺T细胞亚群分化的调节作用进行综述。

To investigate the phenotype and function of macrophages in systemic lupus erythematosus (SLE) patients and normal controls, CD14⁺ monocytes were isolated from the peripheral blood of SLE patients and healthy controls(HC) matched for age and sex. We cultured human monocytes for 7 days with macrophage colony-stimulating factor (M-CSF) to generate macrophages. The CD163 expression was detected by FACS. CD4⁺T cells were isolated from peripheral blood mononuclear cells (PBMC) of one healthy donor, and then were cocultured with macrophages from SLE or HC in a ratio of 5:1 with anti-CD3/CD28 stimulation for 4 days. The proliferation of T cells was detected by FACS. To determine the phagocytic activity of SLE macrophages, apoptotic cells were added into the cultures for 2 hours. The uptake of apoptotic cells was determined by FACS. Compared with HC macrophages, SLE macrophages exhibited lower expression of CD163. The immunomodulatory function of SLE macrophages was also impaired. SLE macrophages could not effectively suppress the proliferation of CD4⁺T cells. The phagocytic activity of SLE macrophages was deficient in engulfment of apoptotic cells. These findings suggest that SLE macrophages are deficient both in phenotype and function.

肥大细胞是来源于骨髓造血干细胞的免疫细胞，广泛分布于机体与外环境交界处如皮肤、胃肠道和呼吸道等部位，不仅参与宿主防御、固有和适应性免疫、免疫自稳和免疫调节，且在过敏性疾病、寄生虫感染、自身免疫病、器官纤维化、血栓与止血中起重要作用。肥大细胞重要特征是当其受外源或内源性物质刺激时，可部分或完全脱颗粒，通过释放的颗粒物质发挥相应的功能。这些预先形成的颗粒主要含蛋白聚糖、蛋白酶、生物胺、溶酶体酶、细胞因子、生长因子等。对肥大细胞预形成颗粒的产生、成熟、脱颗粒机制及其主要颗粒的成分进行研究，将有助于揭示肥大细胞在健康和疾病中的作用。

放疗一直是恶性肿瘤的重要治疗手段之一，但是肿瘤的放疗抵抗却非常普遍，常常导致治疗失败。近几年来肿瘤免疫疗法进展迅速，免疫检查点抑制剂抗肿瘤效果令人瞩目。研究发现放疗联合应用免疫检查点抑制剂可产生抗肿瘤协同作用，甚至使对单一治疗抵抗的肿瘤转为对联合治疗敏感。本文对相关研究进行综述，为未来的临床应用提供思路。

The aim of this study is to explore the correlation of clinical stages and the immune status with the level of myeloid-derived suppressor cells (MDSC) in the peripheral blood in patients with non-small cell lung cancer (NSCLC). Blood samples were collected from peripheral vein of 116 patients with NSCLC and 30 healthy volunteers. The ratios of MDSCs and Tregs in PBMC were detected by flow cytometry and the relationships with clinical stages, pathological types as well as the immunity were also researched. The results showed that compared with the healthy group, the rates of G-MDSC and M-MDSC in NSCLC were significant elevated (P<0.05); G-MDSC and pathological types were correlated with clinical stages (n=116, r=0.330, P<0.001; n=116, r=0.441, P<0.001). There was no correlation between the clinical stages and M-MDSC or Tregs (n=116, r=0.053, P=0.558; n=116, r=0.173, P=0.052). The G-MDSC correlated highly with Tregs (n=116, r=0.343, P<0.001), and so with the pathological types (r=0.333, P<0.001). The M-MDSC had no correlation with Tregs (r=0.333, P<0.001) or pathological types (r=-0.143, P=0.109).The level of MDSC in the peripheral blood of NSCLC patients was increased. Furthermore, G-MDSCs were found to have a positive correlation with clinical stages of NSCLC and Tregs. The results indicate that regulating the expression of MDSC may generate a new strategy for preventing occurrence of NSCLC and postoperative recurrence and metastasis [NCT02603003].

TLR2 is a member of the TLR family, which recognizes PAMP as well as damage-associated molecular pattern (DAMP). TLR2 signaling pathway can regulate the phenotype and function of a wide array of immune cells like DC, macrophage, NK cell, T cell, mast cell to enable them to perform more effectively anti-pathogen and anti-tumor functions. Recently, researches about the involvements of TLR2 in the development and treatment of many diseases progress rapidly and become the potential target for many diseases. This review summarized comprehensively multiple roles of TLR2 in immune responses at the cellular, molecular and functional levels.

新近的研究结果表明，当机体受到病原微生物感染､应激等刺激时，细胞的线粒体会由于活性氧(ROS)的积累､钙离子的异常等发生损伤，受损的线粒体与线粒体双磷脂酰甘油､线粒体抗病毒信号蛋白(MAVS)等通过调控炎性小体的形成，进而影响含半胱氨酸的天冬氨酸蛋白水解酶1(Caspase-1)依赖的炎性细胞因子如白细胞介素1β(IL-1β)和白细胞介素18(IL-18)等的分泌以及细胞焦亡(pyroptosis)的发生，在机体抵抗感染的发生发展中发挥重要作用。本文将着重探讨线粒体在炎性小体激活过程中的双向调节作用。

中性粒细胞是人体重要的免疫细胞。近期发现其在肿瘤发生、发展中发挥一定作用，对其深入研究有利于肿瘤患者免疫状态评估，后者对肿瘤的免疫治疗和传统治疗均有指导意义。本文对近五年中性粒细胞的研究现状进行了整理，对其在肿瘤发生、发展中的作用作了较为全面的陈述。

金属元素在很多生命过程中都发挥重要的作用，是人体中必不可少的成分。许多金属元素在免疫系统中的应用已具有较长的历史。金属免疫学是研究金属离子及其化合物参与免疫细胞发育、免疫应答和免疫调控等过程的学科。金属免疫学这个概念的提出，使人们对金属元素在免疫学中的重要性有了更全面和深入的认识。近年来，许多关于金属元素在免疫系统中的功能的研究成果令人振奋。该文简述了锰、钙、铁和锌等几种常见金属元素在免疫系统中的功能，提出了锰作为危险相关分子模式（danger-associated molecular pattern, DAMP）或警报素的工作模型并阐述其作为天然免疫激动剂的实际应用，最后对金属免疫学的发展进行了展望。

Notch信号通路在进化上十分保守，通过介导细胞之间的相互作用贯穿于机体的各项生命活动，精细地调控生长、发育、凋亡等过程的进行。调节性T细胞是一类表型和功能特异的T细胞亚群，通过与靶细胞直接接触或分泌抑制性细胞因子的方式在维持机体免疫稳态中起重要作用。本文重点对Notch信号通路调控调节性T细胞分化与功能的研究进展进行综述。

Schistosoiasis japonicum(SJ)is a widely distributed chronic parasitic zoonoses caused by Schistosoma. This study was to explore the changes of phenotypes among different innate immune cells in the mesenteric lymph nodes after SJ infection. Mesenteric lymphocytes were isolated from C57BL/6 mice infected with SJ for 6 weeks，and cell surface staining was done. It was found that the absolute number of γδT，NK and NKT cells from the MLNs of the infected mice was significantly higher compared with normal mice (P < 0.05), but the percentage of NK cells increased (P<0.05). In addition, γδT，NK and NKT cells from LN of the infected mice expressed higher level of CD69 (P < 0.01). Moreover, we found that the expression of CD4 was increased in γδT and NK cells in infected MLN (P < 0.05), indicating that these two kinds of cells might play roles in modulating the classical T cell response. Finally, our results showed the expressions of CD94 and CD314 in NK cells, and CD314 in NKT cells was decreased, suggesting that the down-regulation of KIR expression might serve as a mechanism in NK and NKT cells activation. Taken together, there are remarkable differences in phenotype between the 3 types of innate immune cells studied in mice infected with Schistosoiasis japonicum.

The assay for transposase-accessible chromatin using sequencing is a new epigenomic technique that detects the profiling of open chromatin landscape. To build a practicable method for human primary immune cells, conditions for cell lysis were tested. 0.1% NP-40 was the most appropriate condition that could lyse cells mildly but thoroughly. Tn5 transposases were used to cut off DNA and load sequencing adapters simultaneously. Following transposition step, library was prepared using PCR amplification. The distribution of insert fragment showed the interval of approximately 200 bp, which was analyzed with Agilent 2100 Bioanalyzer. Using bioinformatic tools to ensure the library quality, the total mapping rate was more than 94%, and mitochondrial DNA percentage was less than 38%, the signal of ATAC-seq was enriched at transcriptional start sites and the overlap between technical repetitions was approximately 80%. In conclusion, we made a high quality library evaluated multidimensionally and it is an ideal ATAC-seq method for processing human primary immune cells.

Gut microbiota dysbiosis exists in patients with different types of cancer, including melanoma, breast cancer, brain glioma, and other parenteral solid tumors. Dysregulated gut microbiota induces the formation of immunosuppressive tumor microenvironment through a variety of mechanisms, causes the occurrence of tumor immune escape, and affects the host's responses to immune checkpoint inhibitors (ICI). The regulatory effects of gut microbiota can enhance the function of immune killer cells and inhibit tumor progression. This review summarizes the regulatory effect of gut microbiota on the progression of parenteral solid tumors and the underlying immunological mechanisms, so as to provide insights for further basic research and clinical application. 

补骨脂为豆科植物补骨脂的干燥成熟果实，含香豆素类、萜酚类、黄酮类等多种活性成分。补骨脂不仅具有促进骨形成、抗肿瘤、抗炎、雌激素样等多种作用，近年来研究表明补骨脂在免疫系统中也发挥了重要的调节作用。本文就补骨脂在免疫器官、免疫细胞、细胞因子、超敏反应、肿瘤免疫和移植免疫等方面发挥的调节作用进行综述。

This study aims to develop a method to efficiently and stably induce the differentiation and expansion of human myeloid-derived suppressor cells (MDSC) in vitro and provide new experimental technology for the study of the function and mechanism of human MDSC. For this purpose, PBMC of healthy volunteers were isolated with Ficoll density gradient centrifugation. Next, monocytes were separated by anchoring technique. PBMC or monocytes were stimulated with GM-CSF and IL-6 (10, 20, 40, 80 ng/mL each) for 4, 7, 14, and 21 days before co-culturing with PBMC for 3 days. The proliferation of CD33⁺ MDSC and T cells and the proportion of CD3⁺IFN-γ⁺ T cells were detected by FACS. The results showed that the PBMC or monocytes were induced to differentiate to less CD33⁺MDSC by conventional methods. However, by improved methods, the monocytes cultured with GM-CSF and IL-6 (each 80 ng/mL) for 14 days (refreshing the culture solution every 4-5 days) were induced to differentiate more efficiently into a higher proportion of CD33⁺MDSC, which showed significant inhibition of T cell proliferation and IFN-γ secretion. This study suggests that with the improved method, the monocytes are efficiently induced to differentiate into CD33⁺ MDSC, which has significant suppressive function.

Pyroptosis is a new research frontier and it plays key roles in inflammatory and immune response. Pyroptosis is involved in the development of a variety of diseases. This review summarizes the up-to-date research progress on the mechanisms of pyroptosis and pyroptosis-related diseases, providing a systematic and comprehensive overview of current knowledge in pyroptosis.

血小板除具有良好的止血功能外，还能积极参与对微生物等外来物质的免疫反应。血小板在平衡清除细菌和诱导免疫应答方面作用复杂。血小板通过特异性受体和颗粒释放与免疫细胞相互作用。近年来，对血小板如何将环境变化传递给其他循环细胞方面的研究取得了许多进展。现对相关研究综述如下。

IFN刺激基因15（interferon-stimulated gene 15， ISG15）编码的蛋白ISG15是最早被发现的一种类泛素蛋白，在生物体内以单体和复合体形式存在。和泛素一样，ISG15的单体和其共价修饰的蛋白参与并调节了复杂的生物学过程。在病毒、细菌感染以及肿瘤发生过程中，ISG15单体和底物蛋白的共价修饰水平均出现不同程度改变，这表明ISG15在固有免疫的调控中发挥重要作用。越来越多的研究表明ISG15和其共价修饰系统已成为疾病预防和治疗的重要靶点。文章介绍了ISG15的发现、结构特点以及其共价修饰系统，并阐述了近年来ISG15在抗病毒、抗菌和肿瘤发生过程中的重要作用。