哮喘患者白细胞介素(IL)-12和IL-13的变化及糖皮质激素对其的影响

目的　观察哮喘患者血清中白细胞介素 (IL) 12和IL 13水平的变化及糖皮质激素对其的影响。方法　采用ELISA法分别检测中度哮喘急性发作期患者 (2 5例 )口服泼尼松治疗 1周前后、缓解期患者 (2 0例 )和健康对照组者 (15例 )血清中IL 12和IL 13水平 ,并同时测 1秒钟用力呼气容积(FEV1)占预计值的百分比和气道阻力 (R5)占预计值的百分比。结果　IL 12水平急性发作期治疗前[(5 8 5± 14 2 )ng/L]较缓解期 [(71 3± 16 2 )ng/L]为低 (P <0 0 5 ) ,与健康对照组 [(85 5± 13 1)ng/L]、急性发作期治疗后 [(79 3± 19 1)ng/L]比较 ,差异均有显著性 (P <0 0 1)。IL 13水平急性发作期治疗前 [(131 3± 2 8 4 )ng/L]较缓解期 [(113 1± 2 6 5 )ng/L]为高 (P <0 0 5 ) ,与健康对照组 [(92 3± 14 4 )ng/L]、急性发作期治疗后 [(84 1± 19 8)ng/L]比较 ,差异均有显著性 (P <0 0 1)。FEV1占预计值的百分比下降和R5占预计值的百分比升高 (P <0 0 1)。直线相关分析表明 ,血清中IL 12与FEV1占预计值的百分比呈正相关 (r=0 4 85 ,P <0 0 5 ) ,与R5占预计值的百分比呈负相关 (r =- 0 5 16 ,P<0 0 5 ) ,与IL 13呈负相关 (r =- 0 5 4 9,P <0 0 1) ;IL 13与FEV1占预计值的百分比呈负相关 (r =- 0 4 93,P <     

IL-13基因+2044G/A多态性与哮喘、血浆细胞因子水平间关系

目的　探讨血浆 Ig E、白细胞介素 13基因 (IL - 13)水平在哮喘以及 IL - 13基因及 2 0 4 4位点具有相同基因型的个体二者的相关性。方法　用聚合酶链反应和限制性片段长度多态性 (PCR/ RFIP)方法检测哮喘对照组 2 0 4 4位点多态性 ,用酶联免疫吸附法 (EL ISA)测定血浆 Ig E、IL - 13水平。结果　 IL - 13基因 2 0 4 4位点存在三种基因型。在哮喘和对照组 ,同一位点具有相同基因型的个体 ,其细胞因子水平存在显著性差异 ,(P<0 .0 1) ,在哮喘或对照组 ,具有相同基因型的个体 ,其 Ig E及 IL - 13水平存在显著性正相关 (r=0 .5 2～ 0 .6 7,P<0 .0 1～ 0 .0 5 )。结论　Ig E、IL - 13是影响哮喘发病的重要细胞因子 ,且二者存在显著性正相关     

特发性肺纤维化患者肺泡灌洗液及血清中前列腺素E2和白细胞介素12、13水平变化的意义

目的　探讨特发性肺纤维化 (IPF)患者肺泡灌洗液及血清中前列腺素E2 (PGE2 )和白细胞介素 12、13(IL 12、IL 13)水平变化的意义。方法　用放射免疫法及酶联免疫吸附法 ,检测 30例IPF患者 (IPF组 )血清及支气管肺泡灌洗液 (BALF)中PGE2 和IL 12、IL 13的水平 ;健康非吸烟的自愿献血者 30名 ,为血清对照组 ,检测其血清PGE2 和IL 12、IL 13的水平 ;以胸痛为主诉进行BALF检查证实为健康者 9名 ,作为BALF对照组 ,检测其BALF中PGE2 和IL 12、IL 13的水平。结果　IPF组患者BALF中PGE2 为 (5 91± 88)ng/L、IL 12为 (1 34± 0 2 5 )ng/L、IL 13为 (38± 5 )ng/L ,对照组BALF中PGE2 、IL 12、IL 13分别为 (2 38± 7)、(2 2 9± 0 2 6 )、(2 0± 4 )ng/L ,两组相比差异有显著意义 (P值均 <0 0 1) ;血清IL 13水平的变化与BLAF一致 ,但IPF组患者血清PGE2 为 (2 35± 13)ng/L、IL 12为 (2 35± 0 14 )ng/L ,与血清对照组相比差异无显著性 (P >0 0 5 )。结论　IPF患者BALF中PGE2 水平升高 ,可能与IL 13的增高和IL 12水平的下降有关 ,并在IPF的发生、发展中起重要的作用。肺纤维化患者PGE2水平增高主要发生在肺的局部 ,而并非全身性的。     

老年支气管哮喘患者IL-18、IL-12水平的变化及临床意义

目的 探讨老年支气管哮喘患者外周血白细胞介素18(IL-18)和IL-12的变化及其在哮喘发病机制中的作用.方法 采用ELISA法检测42例老年支气管哮喘患者及26例正常对照组检测血清中IL-18及IL-12水平.结果 支气管哮喘发作期患者的血浆IL-12明显高于正常对照组(P<0.01),IL-18明显高于正常对照组(P<0.01).结论 IL-18、IL-12参与了老年支气管哮喘发作期的发病机制,IL-18、IL-12在Th1/Th2细胞因子网络失衡的发病机制中起重要的调节作用.     

白细胞介素13基因-1112C/T多态性与支气管哮喘患者发病及血浆总IgE水平的相关性

目的探讨白细胞介素13(IL13)基因启动子区-1112C/T多态性与支气管哮喘(简称哮喘)的相关性及对血浆总IgE水平的影响。方法将哮喘患者(100例)和健康人(100名)被分为哮喘组和对照组,用聚合酶链反应限制性片段长度多态性(PCRRFLP)方法检测哮喘组与对照组-1112位点多态性,用酶联免疫吸附法(ELISA)测定血浆总IgE水平。结果-1112位点等位基因C、T频率在两组间分布的差异具有显著性(χ2=901,P<001),等位基因T与哮喘关联[OR(T/C)=203,95%CI=127～323,P<001]。两组基因型(TT、CT、CC)频率的分布比较差异有显著性(χ2=719,P<005),其优势比OR(TT/CC)=299,95%CI=106～841(P<005);OR(CT/CC)=204,95%CI=109～381(P<005);OR(TT/CT)=146,95%CI=049～437(P>005);在哮喘组CC、CT及TT基因型患者的血浆总IgE水平分别为(204±89)kU/L、(320±108)kU/L、(376±147)kU/L,而在对照组CC、CT及TT基因型患者的血浆总IgE水平分别为(96±34)kU/L、(122±42)kU/L、(150±36)kU/L。同组内T等位基因携带者血浆总IgE水平高于非携带者;同一基因型中哮喘组总IgE水平高于对照组。结论IL13基因-1112位点多态性是影响哮喘的重要候选基因,T等位基因与哮喘关联,并可能通过增强IL13基因的表达影响血浆总IgE水平。     

囊尾蚴病患者IL-4、IL-5和IL-10水平检测

目的探讨白细胞介素4(IL-4)、白细胞介素5(IL-5)和白细胞介素10(IL-10)在囊尾蚴病发病中的免疫学作用。方法用双抗体夹心(ELISA)法检测囊尾蚴病患者血清中IL-4、IL-5和IL-10水平。结果囊尾蚴病患者血清中IL-4、IL-5和IL-10水平分别为(152.3±31.2)、(256.4±23.3)和(343.9±20.8)ng/L,正常对照组血清中IL-4、IL-5和IL-10水平分别为(75.0±28.5)、(119.5±17.6)和(106.7±19.6)ng/L,2组比较差异均有统计学意义(t值分别为10.6、27.1和48.4,P<0.001)。结论囊尾蚴感染患者Th2型细胞因子表达水平失常,体液免疫功能升高,说明囊尾蚴感染可致宿主免疫功能紊乱。     

急性冠状动脉综合征患者血清IL-10及IL-12水平测定

目的 :探讨白细胞介素 - 10 (IL- 10 )、白细胞介素 - 12 (IL- 12 )对动脉粥样硬化 (AS)形成和发展的影响。方法 :分别对 18例急性心肌梗死 (AMI)患者于发病当天及第 3,5 ,7,10 ,14天 ;14例不稳定型心绞痛 (UAP)患者及 10例健康对照者测定血清 IL - 10、IL - 12水平。结果 :1U AP患者 IL - 10、IL - 12水平显著高于对照组。 2A MI患者血清 IL - 10于发病当天至第 5天显著高于其他两组 ,并于第 3天达高峰。 IL - 12于发作当天及第 10～ 14天显著高于对照组。3AMI死亡组 IL - 10水平明显高于生存组 ,而 IL - 12无显著性差异。结论 :提示急性冠状动脉事件患者 IL - 10、IL - 12升高 ,二者可能参与了 A S的形成和发展 ,并可作为急性期预测指标。     

法舒地尔对支气管哮喘小鼠肺组织Rho激酶-1表达及气道炎症的影响

目的 观察Rho激酶-1抑制剂法舒地尔对支气管哮喘(简称哮喘)小鼠肺组织Rho激酶-1表达及气道炎症的影响,探讨Rho激酶-1在哮喘气道炎症中的作用机制.方法 将24只BalB/c小鼠采用随机数字表法分为对照组、哮喘组和干预组,每组8只.哮喘组、干预组小鼠分别给予卵清白蛋白(OVA)致敏和激发.每次雾化前1 h,干预组给予法舒地尔(10 mg/kg)腹腔注射.末次激发后收集BalF,离心后计数细胞总数及嗜酸粒细胞(EOS)数量.ELISA法测定BalF上清液中嗜酸粒细胞趋化因子(Eotaxin)、白细胞介素(IL)-5和IL-13水平.肺组织HE染色.采用逆转录PCR和免疫组织化学测定各组小鼠肺组织中Rho激酶-1 mRNA和蛋白的表达水平.结果 (1)哮喘组BalF中细胞总数及EOS数量分别为(1.45±0.12)× 10~9/L和(0.52 ±0.06)× 10~9/L,明显高于对照组[分别为(0.58±0.06)×10~9/L和(0.01±0.01)×10~9/L](q值分别为25.909和35.002,均P＜0.01)和干预组[分别为(0.89 ±0.09)×10~9/L和(0.20±0.04)×10~9/L](q值分别为16.676和21.537,均P＜0.01).(2)哮喘组Eotaxin、IL-5及IL-13水平分别为(45±8)ng/L、(157 ±23)ng/L和(429±46)ng/L,明显高于对照组[分别为(10 ±3)ng/L、(26±6)ng/L和(126 ±20)ng/L](q值分别为18.246、23.009、25.826,均P＜0.01);干预组分别为(20±5)ng/L、(57 ±14)ng/L和(254±28)ng/L,明显低于哮喘组(q值分别为13.119、17.503、8.449,均P＜0.01).(3)对照组小鼠气道周围无炎症细胞浸润,哮喘组小鼠气道黏膜水肿,气道壁及管周有大量以EOS为主的炎症细胞浸润,干预组气道炎症反应较哮喘组减轻.(4)哮喘组肺组织Rho激酶-1 mRNA和蛋白的表达水平明显高于对照组(q值分别为25.614和8.156,均P＜0.01),干预组Rho激酶-1 mRNA和蛋白表达水平低于哮喘组(q值分别为20.379和4.135,均P＜0.01).(5)Rho激酶-1 mRNA表达量与BalF中EOS数量、Eotaxin、IL-5和IL-13水平呈正相关(r值分别为0.709、0.600、0.613、0.650,均P＜0.01).结论 Rho激酶-1参与过敏原诱导的哮喘小鼠气道炎症的发生,应用法舒地尔抑制其表达和活性可能改善哮喘气道炎症.     

子宫内膜癌患者血清VEGF、IL-8、IL-24水平变化及意义

目的 观察子宫内膜癌患者血清血管内皮生长因子( VEGF)、白细胞介素8(IL-8)及白细胞介素24( IL-24)的变化,并探讨及意义.方法 采用流式细胞术检测40例子宫内膜癌患者(观察组)和40例健康对照者(对照组)血清VEGF、IL-8及IL-24.结果 观察组血清VEGF、IL-8及IL-24分别为(592.48±131.61)ng/L、(50.15±2.37)pg/mL、(0.75±0.15) ng/mL,对照组分别为(239.35±58.37 ng/L、(34.60±2.61) pg/L、(0.58±0.13)ng/mL,两组相比P均＜0.05.观察组Ⅰ期者血清VEGF、IL-8及IL-24分别为(443.53±127.14) ng/L、(41.32±1.67)pg/mL、(0.68 ±0.11) ng/mL,Ⅱ期者分别为(581.62±121.56) ng/L、(48.31±2.17) pg/mL、(0.74±0.14) ng/mL,Ⅲ期者分别为(704.25±217.33) ng/mL、( 57.41±1.83) pg/mL、(0.81±0.12) ng/mL,Ⅳ期者分别为(916.41±407.32) ng/L、(64.28±2.58) pg/mL、(0.90±0.10) ng/mL.血清VEGF、IL-8及IL-24随着子宫内膜癌临床分期的升高而升高(r分别为0.69,、0.72、0.65,P均＜0.01).结论 子宫内膜癌患者血清VEGF、IL-8、IL-24表达升高.检测子宫内膜癌患者血清VEGF、IL-8、IL-24有助于判断患者病情.     

支气管哮喘患者血浆白细胞介素-6和γ-干扰素的变化

目的　观察支气管哮喘患者血浆白细胞介素 - 6 (interleukin- 6 ,IL - 6 )及γ-干扰素 (interferon-γ,IFN-γ)与哮喘的病情程度之间的关系。方法　测定 2 4例支气管哮喘患者急性发作期治疗前后血浆 IL- 6与 IFN- γ水平 ,与2 5例健康对照组比较。结果　哮喘急性发作期血浆 IL- 6水平高于对照组 ,临床缓解期仍高于对照组。哮喘急性发作期血浆 IFN- γ水平低于对照组 ,临床缓解期升至 (38.4± 13.8) pg/ ml。哮喘急性发作期 IL- 6 / IFN- γ比值 (6 .9±3.2 )高于对照组 (3.4± 1.7) ,差异具有显著性 (P<0 .0 1) ,临床缓解期有所下降 ,但仍高于对照组。结论　支气管哮喘时存在着 IL - 6与 IFN-γ平衡失调 ,T辅助细胞亚群失衡在哮喘发病中起着重要的作用。     

Serum IL-4, IL-10 and IL-6 levels in inflammatory arthritis

As the available in vitro and in vivo data suggest that interleukin (IL)-4 and IL-10 have immunosuppressive activity, our hypothesis was that serum IL-4 and IL-10 levels would correlate inversely with parameters of inflammation in patients with inflammatory arthritis. IL-4 was detected in the serum of 12 out of 140 patients with rheumatoid arthritis (RA), which was increased compared to the proportion found with patients with osteoarthritis (OA; P< 0.02). In addition, IL-4 was detected in the serum of 2 of 19 patients with systemic lupus erythematosus (SLE), 2 of 24 patients with psoriatic arthritis and 1 of 5 patients with Behçet's syndrome. No IL-4 was detected in patients with the following conditions: OA (58 patients), gout (17 patients), ankylosing spondylitis (6 patients), Reiter's syndrome (6 patients), polymyalgia rheumatica (6 patients), temporal arteritis (5 patients) and scleroderma (3 patients). No IL-10 was detected in any of the sera tested. We discuss the possible relevance of these results to the regulation of the immune response evident in inflammatory arthritis.     

DOWN-REGULATION OF FIBRINOGEN BIOSYNTHESIS BY IL-4, IL-10 AND IL-13

High levels of fibrinogen are recognized as an important vascular risk factor; however, it is not known if the increase of plasma fibrinogen is directly responsible for this risk, or is only a marker of vascular inflammation. To support this second hypothesis, Oncostatin M (OSM) is a potent stimulator of fibrinogen biosynthesis and induces smooth muscle cell proliferation. In the same way, we analysed whether interleukin-4 (IL-4), interleukin-10 (IL-10) or interleukin-13 (IL-13), which protect vessel walls from monocytes injuries leading to atherosclerosis, could influence fibrinogen biosynthesis. The two levels of regulation of fibrinogen biosynthesis were tested: firstly, the direct effect of these cytokines on fibrinogen production by the hepatoma cell line Hep G2, and secondly their effect on the secretion of hepatocyte stimulating factor (HSF) activity in the supernatant of lipopolysaccharide (LPS)-activated monocytes. IL-4 and IL-13 added to Hep G2 cells down-regulated both the increase of fibrinogen secretion induced by IL-6 and fibrinogen mRNA levels, this effect being more pronounced when Hep G2 were preincubated with the two cytokines before IL-6 addition. The effect of IL-10 was evidenced only on mRNA expression. IL-10 and IL-13 dose-dependently decrease HSF activity secreted by LPS-activated monocytes, whereas IL-4 had no effect. However, the three cytokines decreased HSF activity when monocytes were incubated with the cytokines before LPS activation. The effects of these cytokines on HSF activity are related to variations of IL-6 and OSM secretion. Our data strengthen the hypothesis that the fibrinogen level is a marker of vascular disease, since cytokines which have a protective vascular effect down-regulate fibrinogen production.     

白细胞介素10基因转染对小鼠心脏移植排斥反应中细胞因子表达的影响

目的 :探讨白细胞介素 10 (IL 10 )基因转染对小鼠心脏移植排斥反应中IL 12、IL 15、IL 18和IL 4表达的影响。方法 :采用小鼠颈部心脏移植模型 ,随机分为 3组 :对照组、移植组和IL 10组。于术后第 5天取移植心脏 ,用逆转录聚合酶链式反应 (RT PCR)法观察IL 12、IL 15、IL 18、IL 4及IL 10的表达情况。结果 :移植组IL 12、IL 15、IL 18表达与对照组比较明显升高 ,IL 10、IL 4表达显著降低 (均P <0 .0 1)。IL 10组IL 12、IL 15、IL 18表达与移植组比较明显降低 ,而IL 4及IL 10表达显著升高 (均P <0 .0 1)。结论 :IL 10基因转染抑制心脏移植排斥反应主要与其抑制IL 12、IL 15、IL 18等Th1型细胞因子的表达 ,促进Th2型细胞因子IL 4的表达 ,使免疫反应由Th1型向Th2型偏移有关     

Expression of IL-23 and IL-17 and effect of IL-23 on IL-17 production in ankylosing spondylitis

The objective of this study was to investigate the expression of IL-23 and IL-17 and the influence of IL-23 on IL-17 production in ankylosing spondylitis (AS) patients. IL-23 and IL-17 levels in the serum and supernatants of cultured peripheral blood mononuclear cells (PBMCs) were determined by ELISA. IL-23p19 mRNA expression in PBMCs were analyzed using RT-PCR. The patients with AS at active stage showed elevated levels of IL-23 and IL-17 in the serum and supernatants of cultured PBMCs. A higher expression of IL-23p19 mRNA in PBMCs of AS patients was also observed. A significantly enhanced production of IL-17 in the supernatants of cultured PBMCs was found in the presence of recombinant IL-23 and this effect was more significant in patients with AS. The results suggest that IL-23 and IL-17 may play critical roles in the pathogenesis of AS and IL-23-stimulated production of IL-17 by PBMCs may be responsible for the development of AS.     

IL-12及IL-10在桥本甲状腺炎发病机制中作用的研究进展

桥本甲状腺炎是一种常见的慢性自身免疫性疾病,表现为辅助性T细胞(Th)1占优势。 Th1类细胞因子白细胞介素(IL)-12表达增加,在该病的诱发及慢性迁延中起重要作用,Th2类细胞因子IL-10表达的下调也与该病有关,且随病情变化二者表达水平有所不同。因此,这些细胞因子可作为病情变化的监测指标,并且可通过调节细胞因子的表达水平从而使失衡的Th1／Th2细胞趋于平衡。这可能为桥本甲状腺炎的治疗开拓一条新途径。     

A complex of the IL-1 homologue IL-1F7b and IL-18-binding protein reduces IL-18 activity

IL-1F7 was discovered in expressed sequence tag databases as a member of the increasing family of proteins sharing sequence homology to IL-1alpha/beta, IL-1Ra, and IL-18. In the present study using immunohistochemical staining, IL-1F7 was localized in human peripheral monocytic cells, suggesting its role in immune regulation. Recombinant human IL-1F7b was shown to bind to the IL-18Ralpha but without IL-18 agonistic or antagonistic function. Using chemical cross-linking, we observed that, unlike IL-18, IL-1F7b fails to recruit the IL-18Rbeta chain to form a functionally active, ternary complex with the IL-18Ralpha chain. IL-1F7b shares two conserved amino acids with IL-18 (Glu-35 and Lys-124), which participate in the interaction of IL-18 with the IL-18Ralpha chain as well as the IL-18-binding protein (IL-18BP), a secreted protein that neutralizes IL-18 activity. In testing whether IL-1F7b interacts with IL-18BP, we unexpectedly observed that IL-1F7b enhanced the ability of IL-18BP to inhibit IL-18-induced IFNgamma by 25-30% in a human natural killer cell line. This effect was observed primarily at limiting concentrations of IL-18BP (3.12-12.5 ng/ml) and at a 50- to 100-fold molar excess of IL-1F7b. Similar results were obtained by using isolated human peripheral blood mononuclear cells. To study the molecular basis of this effect we performed binding studies of IL-1F7b and IL-18BP. After cross-linking, a high molecular weight complex consisting of IL-1F7b and IL-18BP was observed on SDS/PAGE. We propose that after binding to IL-18BP, IL-1F7b forms a complex with IL-18Rbeta, depriving the beta-chain of forming a functional receptor complex with IL-18Ralpha and thus inhibiting IL-18 activity.     

Prognostic values of IL-6, IL-8, and IL-10 in acute pancreatitis

GOALS: The prognostic importance of interleukin-6 (IL-6), IL-8, and IL-10 in the prediction of acute pancreatitis severity. BACKGROUND: Early assessment of severity in acute pancreatitis could help the patients who are at risk of developing complications. Unfortunately, the used prognostic scoring systems generally are only moderately accurate in assessing disease severity. STUDY: We studied 117 consecutive patients with a diagnosis of acute pancreatitis admitted to our hospital during the past 2 years. Laboratory parameters and cytokines were analyzed from serum taken routinely on admission. Severity criteria were noted for each patient using Ranson, Glasgow, and APACHE II scoring systems. Local and systemic complications, developed during a follow-up period, were classified by Atlanta criteria. RESULTS: IL-6 was the only parameter that statistically significantly predicted complicated acute pancreatitis (P<0.05). IL-8 and IL-10 and the 3 prognostic scoring systems used did not properly assess complicated versus noncomplicated acute pancreatitis. CONCLUSIONS: Our prospective study supported the potential importance of IL-6 in the early assessment of complicated acute pancreatitis, but also suggested that pancreatitis classified as complicated in a large number of patients could not be correctly predicted with the Ranson, Glasgow, and APACHE II scoring systems.     

低氧条件下 IL-6、IL-8、IL-10作用机制研究进展

低氧(hypoxia)是机体循环血液中氧分压较低的状态,缺氧则引发机体的一系列反应。随着研究的深入,发现机体内不但存在氧化应激反应,还伴随着一系列炎症反应,IL-6、IL-8、IL-10作为常见的炎症因子也成为研究热点,本文就低氧条件下三种 IL 的作用机制作一总结,为低氧造成的机体损伤提供更多理论依据,为低氧损伤的预防及治疗提供新靶点。     

Whole Tumor Cell Vaccine Adjuvants: Comparing IL-12 to IL-2 and IL-15

Cancer immunotherapy (passive or active) involves treatments which promote the ability of the immune system to fight tumor cells. Several types of immunotherapeutic agents, such as monoclonal antibodies, immune checkpoint inhibitors, non-specific immunomodulatory agents, and cancer vaccines are currently under intensive investigation in preclinical and clinical trials. Cancer vaccines induce permanent activation of the immune system and may be considered the most promising method for cancer treatment, especially in combination with other agents of passive immunotherapy. Among various approaches to cancer vaccines, whole tumor cell vaccines have been attracting attention for several years. Despite their low to moderate clinical effects, these vaccines have numerous advantages. Their ability to generate immune responses against tumor-associated antigens reduces the possibility for tumor cells to escape and facilitates the development of “off-the-shelf” allogeneic tumor vaccines. Understanding the reciprocal interactions between tumor cells and leukocytes is a key to harness the full potential of whole cell vaccination. Cytokines are considered as potent immunomodulatory molecules which behave as adjuvants in whole tumor cell vaccines. Improved mechanistic understanding of key cytokines in tumor immunity will serve as a resource for rational design of whole cell cancer vaccines. Although there are several reports about the use of different immunostimulatory cytokines as adjuvants, interleukin (IL)-12 appears to have superior effects compared to other cytokines. This review describes the effects of IL-12 compared to other immunomodulatory cytokines, such as IL-2 and IL-15, and highlights its application in whole cell tumor vaccination.