旋毛虫Ts87重组蛋白诱导的小鼠黏膜免疫保护性研究

本实验探讨旋毛虫Ts87重组蛋白灌胃免疫小鼠诱导的黏膜免疫保护性作用。实验分对照组、佐剂组(霍乱毒素B亚单位组,CTB)和免疫组(CTB Ts87重组蛋白),灌胃免疫,间隔1周共免疫3次。末次免疫后第7天用400条旋毛虫感染期幼虫攻击,比较3组小鼠肠道成虫数、雌虫生殖力和肌幼虫数。且于末次免疫后第7天刮取肠黏液、取血检测特异性sIgA、IgG抗体水平。结果显示免疫组小鼠成虫减虫率、新生蚴减虫率、肌幼虫减虫率分别是81·34%、67·02%、84·49%;小鼠肠黏液sIgA水平及血清IgG水平显著高于对照组和佐剂组。结果表明Ts87重组蛋白黏膜免疫能够诱导小鼠产生抗旋毛虫的保护性免疫。灌胃免疫能显著提高肠黏液特异性sIgA水平,对促进肠道成虫的排出有明显作用。     

乳酸菌Z222产胞外多糖(EPSⅠ)对免疫细胞功能的影响

目的　检测乳酸菌Z2 2 2 产胞外多糖EPSⅠ对体外免疫细胞功能的调节作用。方法　不同浓度的EPSⅠ作用于小鼠的腹腔巨噬细胞和脾细胞 ,分别用中性红染色法检测巨噬细胞的吞噬能力 ,用MTT法检测淋巴细胞在体外的转化能力、NK细胞杀伤肿瘤细胞Yac 1的能力和产细胞因子IL 2的活性。结果　 (1)EPSⅠ单独作用小鼠脾细胞就能促进体外淋巴细胞增殖 ,且表现出剂量依赖关系。EPSⅠ亦可促进ConA诱导的体外小鼠淋巴细胞转化。 (2 )EPSⅠ体外作用于小鼠腹腔巨噬细胞均可提高MΦ的吞噬能力 ,与对照组比较差异都有显著性。 (3)与对照组相比EPSⅠ能增加体外NK细胞的活性 ,杀伤率最大值达 6 2 .4 1%± 2 .5 4 %。 (4 )EPSⅠ使小鼠脾细胞产IL 2的能力与对照组比较 ,差异有显著性。结论　乳酸菌多糖EPSⅠ对小鼠的免疫功能有一定的调节作用。     

Molecular mechanisms underlying IFN-{gamma}-mediated tumor growth inhibition induced during tumor growth inhibition induced during tumor immunotherapy with rIL-12

The present studnt Investigates the molecular by which IFN-produced as a result of in vitroIL-12 addministration exertsits anty-tumor,rIL-12 was administered three or five times intomice bearing CDA1M fibrosarcoma, OV-HM ovarian carcinoma orMCH-1-A1 fibosarcoma. This regimen induced complete regressionof CSA1M and OV-HM tumors but only transient growth inhibitionof MCH-1-A1 tumors. The anty-tumor effects of Il-12 were associatatedwith enhanced induction of IFN-becouse these effects were abrogatedby pretreatment of hosts with anti-IFN- antibody.Exposure inin vitro of the three types of tumor cells to rIFN- resultedin moderate to potent inhibition of tumor cell growth.IFNstimulatedthe expression of mRNAs for an inducible type of NO synthasa(INOS)in CSA1M cells and indoleamine 2,3-dioxygenasa (IDO),an enzyme capable of degrading tryptophan, in OV-HM cells ,but induced only marginal levels of these mRNAs in MCH-I-ALcells. In association withiNOS gene expression, INF--stimulatedCSA1M cells produced a large amount of NO which functioned toinhibit their own growth in vitro. Although OV-HM and MCH-1-A1cells did not produce NO, they also exhibited NO susceptibility.Whereasthe tumor masses from IL-12-treated CSA1M-bearing mice inducedhigher levels of INOS (for CSA1M) or IDO and iNOS (for OV-HM)mRNAs,the MCH-1-A1 tumor mass expressed lower levels of iNOS mRNAalone.Moreover, massive infiltration of CD4⁺and CD8⁺ T cellsand Mac-1⁺ cells was seen only in the CSA1M and OV-HM tumors.Thus, these results indicate that IFN- produced after IL-12treatment induces the expression of various genes with potentialto modulate tumor cells and growth by acting directly on tumorecells or stimulating tumor-infiltrating lymphold cells and thatthe effectiveness of IL12 therapy is assoiated with the operation if these mechanisms.     

Hypersensitivity pneumonitis in rabbits. Modulation of pulmonary inflammation by long-term aerosol challenge with antigen

Immunized rabbits that were aerosol challenged for 2 to 3 wk with pigeon dropping extract, an etiologic agent of hypersensitivity pneumonitis, developed chronic pulmonary inflammation associated with cell-mediated immunity in bronchoalveolar cells. However, prolonged aerosol challenge for 12 wk resulted in the diminution of pulmonary inflammation (modulation) and the loss of demonstrable cell-mediated immunity. This was probably not due to loss of sensitized lymphocytes that mediated pulmonary inflammation. Furthermore, rabbits undergoing modulation when they were challenged with an unrelated antigen were refractory to the development of pulmonary inflammation for at least 9 wk. After this refractory period, animals reimmunized and aerosol challenged with pigeon dropping extract displayed an anamnestic response and produced pulmonary lesions that were strikingly similar to the histopathology of human hypersensitivity pneumonitis.     

流感病毒免疫防御机制研究进展

流感病毒感染引起免疫损伤的同时可以激发机体产生免疫应答,在病毒的清除与疾病的恢复及再次感染过程中发挥着有效的防御作用.尽管流感病毒经常发生变异,但自然感染诱导的免疫防御机制仍可提供一定程度的交叉保护作用.这一系列免疫应答的激发及形成包括多种分子及细胞的参与,其发生、发展及转归直接决定着疾病的严重程度及免疫预防的有效性.了解天然免疫应答、粘膜免疫应答及获得性免疫应答的激发与维持可为流感病毒的防治及疫苗的研制提供思路.     

Natural killer cells and malaria

Summary:  Malaria, caused by the infection with parasites of the germs Plasmodium , is one of the three most important infectious diseases worldwide, along with tuberculosis and infection with human immunodeficiency virus. Natural killer (NK) cells are lymphocytes classically involved in the early defense against viral infections and intracytoplasmic bacterial infections and are also implicated during the course of tumor development and allogeneic transplantation. These cells display important cytotoxic activity and produce high levels of proinflammatory cytokines. In both mouse and human models of malaria, NK cells appear to be a major source of interferon-γ during the early phase of infection. In humans, indirect signaling through monocytes/macrophages required to optimally stimulate NK cell activity. However, the in vivo functions of NK cells during malaria are still enigmatic, and many issues remain to be dissected, such as the molecular basis of the direct recognition of iRBCs by NK cells.     

用高价人抗HBs在人体内诱导产生抗HBs

本文探讨用外源性人抗HBs在人体通过免疫网络诱导产生自身的抗HBs的可能性。志愿者经多次注射人高价抗HBs(Ab_1)后,体内产生了Ab_2,进而产生出特异性与Ab_1相同的Ab_3;当Ab_3水平升高时,Ab_2水平下降。此结果证实了人体内独特型网络的存在及其活跃的调节功能,表明用于被动免疫的人抗HBs在人体也能通过激活独特型网络产生主动免疫保护作用。此外,本文的结果还提示,注射人抗HBs后,人体内产生的Ab_2可模拟HBsAg,使常规的HBsAg检查出现假阳性结果。     

The effect on immunity of long-term intensive training in elite swimmers

The impact of long-term training on systemic and mucosal immunity was assessed prospectively in a cohort of elite swimmers over a 7-month training season in preparation for national championships. The results indicated significant suppression (P < 0.05) of serum IgA. IgG and IgM and salivary IgA concentration in athletes associated with long-term training at an intensive level. There was also a trend towards lower IgG2 subclass levels in serum in athletes compared with controls (P= 0.07). There were no significant changes in numbers or percentages of B or T cell subsets, but there was a significant fall in natural killer (NK) cell numbers and percentages in athletes over the training season (P < 0.05). After individual training sessions there was a significant decrease in salivary IgA levels for athletes compared with controls (P= 0.02). In athletes there was a downward trend in salivary IgA levels over the 7-month training period in both the pre-exercise (P= 0.06) and post-exercise samples (P= 0.04). There were no significant trends in salivary IgG levels over the study period in either athletes or controls. The only significant change in salivary IgM levels was an increase in detection rate in the pre-competition phase in athletes (P= 0.03). The study suggests that training of elite athletes at an intensive level over both short- and long-time frames suppresses both systemic and mucosal immunity. Protracted immune suppression linked with prolonged training may determine susceptibility to infection, particularly at times of major competitions.     

检测体内异种II型胶原异体移植引起的细胞毒反应

检测用猪II型胶原免疫新西兰大白兔的异种异体细胞免疫反应。用II型胶原免疫新西兰大白兔60 d,定期抽取血浆检测抗II型胶原抗体;第60 d取兔的外周血淋巴细胞、兔脾细胞、淋巴结分别分离淋巴细胞,进行体外二次II型胶原刺激,检测由此引起的反应性的细胞增殖规律。实验分为二组,第一组加入不同浓度植物血凝素(PHA)作阳性对照,并测定非特异性免疫;第二组加入不同浓度II型胶原,检测特异性免疫。正常兔的淋巴细胞在PHA剌激下发生增殖,但对II型胶原的第一次剌激不发生增殖,而免疫兔对PHA和II型胶原的剌激均能发生显著的增殖。表明异种II型胶原在一定浓度下,可以引起免疫兔的抗II型胶原抗体的升高,并可引起兔脾、外周血淋巴细胞增殖,异种II型胶原能在体内引起细胞免疫反应。     

Endomorphin-2 modulates productions of TNF-alpha,IL-1beta,IL-10, and IL-12, and alters functions related to innate immune of macrophages

We evaluate immunological effects of opioid peptide endomorphin-2 on the production of cytokines related to inflammation and Th1/Th2 balance, and functions related to innate immune of rat peritoneal macrophages. Endomorphin-2 inhibited TNF-, IL-10, and IL-12 productions, but potentiated IL-1 production by macrophages. Moreover, endomorphin-2 potentiated macrophage adhesion to fibronectin, and the expression of adhesion molecule Mac-1 on macrophages. In contrast, endomorphin-2 suppressed phagocytosis of opsonized E. coli by macrophages, without affecting phagocytosis of non-opsonized E. coli. In addition, endomorphin-2 inhibited macrophage chemotaxis, and the production of superoxide anion by macrophages. These results suggest that endomorphin-2 may alter macrophage functions such as cytokine productions and functions related to innate immune.