ROLE OF L3T4+ LYMPHOCYTES IN PROTECTIVE IMMUNITY TO SYSTEMIC CANDIDA-ALBICANS INFECTION IN MICE
ROLE OF L3T4+ LYMPHOCYTES IN PROTECTIVE IMMUNITY TO SYSTEMIC CANDIDA-ALBICANS INFECTION IN MICE
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DOI：
10.1128/iai.57.11.3581-3587.1989
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发表时间：
1989-11-01
影响因子：
3.1
通讯作者：
BISTONI, F
中科院分区：
文献类型：
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作者：
CENCI, E;ROMANI, L;BISTONI, F
在经PCA-2处理的小鼠的足垫出现对白色念珠菌的强烈迟发型超敏反应(DTH)时，感染低毒力致病酵母变异株PCA-2的小鼠在体内检测到对致死白色念珠菌攻击的保护性免疫，并在体外检测到具有高杀菌活性的脾巨噬细胞的激活。迟发型超敏反应可移植到这些动物的脾细胞群中，脾淋巴细胞在L3T4+细胞中的浓缩显著增加，导致足底肿胀。由L3T4+细胞转移的反应性是一种辐射敏感现象(体外为2,500 rad)，需要与宿主中耐辐射的二氧化硅敏感的同基因细胞合作，并通过用L3T4抗原抗体或小鼠伽马干扰素处理受体小鼠来抑制。在体外，PCA-2免疫的L3T4+细胞在与白色念珠菌孵育时产生各种淋巴因子活性，包括γ干扰素和粒-巨噬细胞集落刺激因子。抗L3T4单抗处理PCA-2感染的小鼠显著削弱了它们的足垫反应和对白色念珠菌的抵抗力，这表现在抗L3T4处理的小鼠肾脏酵母细胞的恢复增加。这些结果提示，PCA-2诱导的抗念珠菌耐药机制可能与特异性诱导炎性L3T4+T细胞和淋巴因子激活的吞噬效应介导的迟发型超敏反应有关。然而，白念珠菌攻击的PCA-2免疫小鼠的存活率并没有被抗L3T4抗体显著提高，因此可以得出结论，当L3T4+细胞活性不足时，代偿机制导致相当大的抗念珠菌耐药性。
Protective immunity to lethal Candida albicans challenge in vivo and activation of splenic macrophages with highly candidacidal activity in vitro were detected in mice infected with low-virulence agerminative yeast cells of the variant strain PCA-2, at a time when a strong delayed-type hypersensitivity (DTH) reaction to C. albicans occurred in the footpads of PCA-2-treated mice. The DTH reaction was transferable with spleen cell populations from these animals, and enrichment of splenic lymphocytes in L3T4+ cells significantly increased to footpad swelling. The reactivity transferred by L3T4+ cells was a radiosensitive (2,500 rads in vitro) phenomenon that required collaboration with radioresistant, silica-sensitive syngeneic cells in the host and was inhibited by treatment of recipient mice with antibodies to the L3T4 antigen or murine gamma interferon. In vitro the PCA-2-immune L3T4+ cells produced various lymphokine activities upon incubation with C. albicans, including gamma interferon and granulocyte-macrophage colony-stimulating factor. Anti-L3T4 monoclonal antibody treatment of PCA-2-infected mice significantly impaired their footpad reaction and resistance to C. albicans, as shown by increased recovery of yeast cells from the kidneys of anti-L3T4-treated mice. These results suggested that the mechanisms of anti-Candida resistance induced by PCA-2 may involve specific induction of a DTH response mediated by inflammatory L3T4+ T cells and lymphokine-activated phagocytic effectors. However, the survival rate of the PCA-2-immune mice challenged with C. albicans was not significantly modified by administration of the anti-L3T4 antibody, thus allowing for the conclusion that compensatory mechanisms lead to considerable anti-Candida resistance when the activity of L3T4+ cells is deficient.