Antigen-induced protective and nonprotective cell-mediated immune components against Cryptococcus neoformans.

Antigen-induced protective and nonprotective cell-mediated immune components against Cryptococcus neoformans.
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抗原诱导的针对新型隐球菌的保护性和非保护性细胞介导的免疫成分。

DOI:
10.1128/iai.66.6.2632-2639.1998
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发表时间:
1998
影响因子:
3.1
通讯作者:
Adesina,A
Adesina,A
中科院分区:
医学2区
文献类型:
--
作者:
Murphy,JW;Schafer,F;Casadevall,A;Adesina,A

文献摘要

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用两种不同的隐球菌抗原制剂免疫小鼠,一种是完全弗氏佐剂(CFA)中的可溶性培养滤液抗原(Cnef),另一种是热致死的新生隐球菌细胞(HKC),它们产生两种不同类型的活化T细胞。Cnef-CFA诱导负责迟发型超敏反应(DTH)和增强抗隐球菌迟发型超敏反应的CD4+T细胞,而HKC诱导参与抗隐球菌迟发型超敏反应的CD4+和CD8+T细胞和直接杀伤C的活化T细胞。新生肿瘤细胞。这项研究的主要目的是评估两种不同的T细胞图谱中的每一种对viableC挑战提供的保护水平。肿瘤细胞,从而识别哪个激活的T细胞特征提供了更好的保护。用Cnef-CFA免疫的CBA/J小鼠在清除FC的基础上有明显更好的保护反应。与HKC免疫的小鼠或同样感染C的对照小鼠相比,新的肿瘤细胞从组织中转移,存活时间更长,大脑中的病变更少和更小。新形态主义者。两种免疫方案均可诱导抗隐球菌型DTH反应,但均不能诱导抗葡萄糖醛酸氧基甘露聚糖的血清抗体,因此在Cnef-CFA免疫小鼠中观察到的保护作用是由于该方案诱导了T细胞的激活。HKC免疫的小鼠没有表现出比对照组更强的保护作用,也没有扩增细胞。根据我们的发现,我们认为保护性的抗隐球菌T细胞是负责DTH反应的CD4+T细胞和/或放大DTH反应的CD4+T细胞,并且先前已经被证明产生高水平的γ-干扰素和白介素2。我们的结果表明存在保护性和非保护性的细胞介导的免疫反应,并突出了免疫反应TOC的复杂性。新的抗原性。
Mice immunized with two different cryptococcal antigen preparations, one a soluble culture filtrate antigen (CneF) in complete Freund’s adjuvant (CFA) and the other heat-killedCryptococcus neoformanscells (HKC), develop two different profiles of activated T cells. CneF-CFA induces CD4+T cells responsible for delayed-type hypersensitivity (DTH) reactivity and for amplification of the anticryptococcal DTH response, whereas HKC induce CD4+and CD8+T cells involved in anticryptococcal DTH reactivity and activated T cells which directly killC. neoformanscells. The main purpose of this study was to assess the level of protection afforded by each of the two different T-cell profiles against challenge with viableC. neoformanscells, thereby identifying which activated T-cell profile provides better protection. CBA/J mice immunized with CneF-CFA had significantly better protective responses, based on better clearance ofC. neoformansfrom tissues, on longer survival times, and on fewer and smaller lesions in the brain, than HKC-immunized mice or control mice similarly infected withC. neoformans. Both immunization protocols induced an anticryptococcal DTH response, but neither induced serum antibodies to glucuronoxylmannan, so the protection observed in the CneF-CFA immunized mice was due to the activated T-cell profile induced by that protocol. HKC-immunized mice, which displayed no greater protection than controls, did not have the amplifier cells. Based on our findings, we propose that the protective anticryptococcal T cells are the CD4+T cells which have been shown to be responsible for DTH reactivity and/or the CD4+T cells which amplify the DTH response and which have been previously shown to produce high levels of gamma interferon and interleukin 2. Our results imply that there are protective and nonprotective cell-mediated immune responses and highlight the complexity of the immune response toC. neoformansantigens.