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41.
L.N Payne P.C Powell M.C Rennie L.J.N Ross 《Comparative immunology, microbiology and infectious diseases》1978,1(1-2):31-36
Current knowledge of the nature of the antigens and of the host immune responses in vaccinal immunity to Marek's disease is reviewed. It is suggested that a two-step mechanism of resistance operates. The first step involves humoral and cell-mediated responses directed against viral antigens; the second step occurs after challenge with Marek's disease virus and consists of cellmediated responses directed against tumour cells. 相似文献
42.
Spickler AR Roth JA 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2003,17(3):273-281
Vaccine adjuvants are chemicals, microbial components, or mammalian proteins that enhance the immune response to vaccine antigens. Interest in reducing vaccine-related adverse effects and inducing specific types of immunity has led to the development of numerous new adjuvants. Adjuvants in development or in experimental and commercial vaccines include aluminum salts (alum), oil emulsions, saponins, immune-stimulating complexes (ISCOMs), liposomes, microparticles, nonionic block copolymers, derivatized polysaccharides, cytokines, and a wide variety of bacterial derivatives. The mechanisms of action of these diverse compounds vary, as does their induction of cell-mediated and antibody responses. Factors influencing the selection of an adjuvant include animal species, specific pathogen, vaccine antigen, route of immunization, and type of immunity needed. 相似文献
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The studies reviewed here evaluated the role cellular immune system components play in control of brucellosis by conducting comparative studies with brucella-resistant C57BL/10 or C57BL/6 mice and susceptible BALB/c mice. We have shown by both in vitro and in vivo studies that activation of macrophages with interferon-gamma (IFN-γ) is an important factor for control of infection with B. abortus in the mouse model and that the mechanism of anti-brucella activity largely involved reactive oxygen intermediates. Differences in control of the organism by resistant and susceptible mice was not related to inherent differences in the ability of their macrophages to control infection either with or without IFN-γ activation nor was it attributable to NK cells since we found no role for them in control of brucellosis in either mouse strain. However, relative resistance to brucellosis did correlate with increased production of IFN-γ by CD4 T cells during the first weeks after infection while IL-10 contributed to susceptibility in BALB/c mice. Moreover, by 3 weeks post-infection splenocytes from the susceptible BALB/c mice failed to produce IFN-γ and relied on TNF- as well as CD8 T cells to control infection until the end of the plateau phase around 6 weeks post-infection when IFN-γ production resumed and clearance began. In contrast, IFN-γ was crucial for control throughout the infection in the more resistant C57BL/6 mice and the mice died in its absence by 6 weeks post-infection compared to 12 weeks for the more susceptible mice that relied on additional mechanisms of control. In contrast to the IFN-γ knock-out mice, both β2 microglobulin knock-out C57BL/6 mice, which do not express conventional MHC class I molecules and thus cannot present antigen to CD8 T cells, or perforin knock-out C57BL/6 mice, which have no T cell cytotoxic activity, controlled and cleared the infection as well as normal C57BL/6 mice. The hiatus of IFN-γ production in BALB/c mice correlated with very high levels of total IL-12 and it was postulated that the lack of IFN-γ was a consequence of p40 homodimer blocking activity. However, reduction of p40 IL-12 in vivo through administration of indomethacin reduced the infection without a concomitant measurable increase in IFN-γ. Current studies are aimed at elucidating the mechanism of the IFN-γ hiatus. 相似文献
44.
Paracox anticoccidial vaccine was administered to a 7-day-old flock of commercial broiler breeder stock subsequently reared to point-of-lay in the same house. For comparison, three subgroups of another flock of broiler breeders were also vaccinated with Paracox at 7 days of age, reared to 42 days and then transferred to new litter on another farm until point-of-lay. The first subgroup received no further treatment, but the second and third each received a second vaccination with Paracox, either immediately after transfer to the new litter or 42 days after transfer. Using an Eimeria necatrix model, protective immunity was demonstrated by virulent challenge of samples of birds from all groups by the age of 37–40 days (30–33 days after the first vaccination), and was maintained to at least 122–125 days of age, whether the birds remained on the same litter or were transferred to another farm, and whether they received one or two anticoccidial vaccinations. Therefore, there is no disadvantage in transferring birds onto new litter 35 days after a single Paracox vaccination, nor is there any advantage in giving a second vaccination after such a transfer. Vaccinated birds seeded the new litter with oocysts, despite being clinically immune to coccidiosis. A supplementary laboratory experiment showed that birds vaccinated at 8 days of age passed almost no oocysts after a second vaccination at 43 days of age. This indicated that they were not only protected against clinical coccidiosis, but were almost solidly immune to a homologous infection 5 weeks after a single vaccination. Nevertheless, oocysts appeared in the litter of all four groups of commercial breeders throughout the trial, showing that wild-type heterologous infections occurred whether the birds were transferred to new litter or not, but these did not overwhelm the acquired protective immunity and cause clinical coccidiosis. 相似文献
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46.
黄芪多糖对人工感染IBDV雏鸡红细胞免疫功能的影响 总被引:1,自引:0,他引:1
将由未免疫接种腔上囊病疫苗鸡的种蛋孵化而来的160只1日龄海兰白雏鸡随机分为A、B、C和D共4组。A组为对照组,B、C和D组于26日龄时按每只0.3mL的剂量用IBDV攻毒。A、B组未用黄芪多糖(APS)处理,C、D组从攻毒当日起连续胸肌注射APS6d,剂量分别为每只鸡5mg和10mg。分别在21、29、32、35、38日龄时心脏采血1~3mL,测定E—C3bRR、E—ICRR、ERER和ERIR。结果显示,雏鸡感染IBDV后可使E-C3bRR和ERER显著降低(P〈0.01);APS处理组E-C3bRR、E-ICRR、ERER均高于A、B组(P〈0.01),其中D组最高,而ERIR则与A组相似。证实,雏鸡感染IBDV后红细胞免疫功能低下,而APS可显著提高其红细胞免疫功能。 相似文献
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饲料中维生素A水平对凡纳滨对虾生长、饲料利用、体组成成分及非特异性免疫反应的影响 总被引:1,自引:0,他引:1
本文旨在研究5种等氮等能饲料中,维生素A添加水平对凡纳滨对虾(Penaeus vannameiBoone)生长、饲料利用、体组成成分及非特异性免疫反应的影响。试验选用平均初始体重为(0.069±0.005)g的凡纳滨对虾450尾,随机分为5个处理组,每组90尾,每组设3个重复,每个重复30尾。试验采用单因素设计,以维生素A醋酸酯为维生素A源,用添加不同水平维生素A(添加量分别为0、18、365、4和72 mg/kg)的饲料喂养凡纳滨对虾,试验期11周。结果表明:在养殖前4周,饲料中添加维生素A显著促进凡纳滨对虾的生长(P<0.05),提高其对饲料利用效率(P<0.05),而对对虾的成活率不产生显著的影响(P>0.05);第11周的结果表明,饲料中添加维生素A并不能显著影响凡纳滨对虾的生长、饲料利用效率和成活率(P>0.05)。维生素A对对虾体脂肪、蛋白质含量的影响显著(P<0.05),对对虾体水分和灰分含量无显著影响(P>0.05)。维生素A对对虾血清中溶菌酶活力、酚氧化酶活力和血液红细胞数量的影响显著(P<0.05),饲料中未添加维生素A或过量添加(超过36 mg/kg)均导致血清中溶菌酶活力、酚氧化酶活力和血细胞总数显著下降(P<0.0 5),而对血清超氧化物歧化酶活力无显著影响(P>0.0 5)。用折线回归模型分析饲料维生素A添加量与对虾增重率的变化关系,表明在试验前4周,凡纳滨对虾饲料中维生素A的适宜添加量为2 2.5 0 mg/kg;1 1周试验期间,凡纳滨对虾饲料中维生素A适宜添加量为1 8 mg/kg;以溶菌酶、酚氧化酶活力为指标,凡纳滨对虾饲料中维生素A最适添加量为5 9.5 1 mg/kg。 相似文献
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