CD4+ subset expression in murine candidiasis. Th responses correlate directly with genetically determined susceptibility or vaccine-induced resistance.
CD4+ subset expression in murine candidiasis. Th responses correlate directly with genetically determined susceptibility or vaccine-induced resistance.
复制标题
CD4 子集在小鼠念珠菌病中的表达。
DOI：
--
复制
发表时间：
1993
影响因子：
4.4
通讯作者：
Francesco Bistoni
中科院分区：
文献类型：
--
作者：
Luigina Romani;A. Mencacci;E. Cenci;R. Spaccapelo;P. Mosci;P. Puccetti;Francesco Bistoni
以前的工作表明，在杂交（BALB/cCr × DBA/2Cr）F1小鼠的致命性播散性疾病的发展与毒性白色念珠菌全身感染检测强Th 2样反应。然而，一个主要的Th 1样反应和长期的抗真菌保护诱导这些小鼠接种减毒C的活芽生孢子。白色念珠菌菌株。当注射到DBA/2Cr小鼠中时，在本研究中发现一种这样的活疫苗株导致以强Th 2应答为特征的进行性疾病。DBA/2小鼠感染减毒疫苗后，血清IgG 1、伊加和IgE反应升高，脚垫反应减弱或不存在，CD 4+细胞体外持续产生Th 2（IL-4和IL-10）但不产生Th 1（IL-2和IFN-γ）细胞因子，以及嗜酸性粒细胞增多。这是在显着的对比，在类似的感染，H-2-兼容的BALB/cCr小鼠的强烈的Th 1反应和持久的anticandidal保护的发展。因此，我们的数据表明，在C.白色念珠菌感染与遗传决定的易感性或疫苗诱导的抗性相关。此外，这种抗性的遗传控制可能与H-2复合体无关。
Previous work has shown that in hybrid (BALB/cCr x DBA/2Cr)F1 mice the development of a fatal disseminated disease by systemic infection with virulent Candida albicans is associated with the detection of strong Th2-like responses. However, a predominant Th1-like response and long-lived antifungal protection are induced by vaccinating these mice with live blastospores of attenuated C. albicans strains. When injected into DBA/2Cr mice, one such live vaccine strain was found in the present study to result in a progressive disease characterized by strong Th2 responses. Elevated serum IgG1, IgA, and IgE responses, weak or absent footpad reactions, sustained production in vitro of Th2 (IL-4 and IL-10) but not Th1 (IL-2 and IFN-gamma) cytokines by CD4+ cells, and eosinophilia were all detected in DBA/2 mice after infection with the attenuated vaccine. This was in marked contrast with the development of strong Th1 responses and persistent anticandidal protection in similarly infected, H-2-compatible BALB/cCr mice. Therefore, our data suggest that the type of Th response that predominates in mice after C. albicans infection correlates with genetically determined susceptibility or vaccine-induced resistance. Moreover, the genetic control of this resistance may not be associated with the H-2 complex.