Wang Y, Li S P, Moser S A, Bost K L, Domer J E
Department of Microbiology and Immunology, Tulane University Medical School, New Orleans, Louisiana 70112-2699, USA.
Infect Immun. 1998 Apr;66(4):1384-91. doi: 10.1128/IAI.66.4.1384-1391.1998.
Candida albicans mannoprotein (MAN) administered intravenously to mice stimulates the production of splenic CD8+ effector cells which downregulate delayed hypersensitivity (DH) in immunized mice. Cytokine involvement in the induction and/or elicitation of downregulation was studied by (i) examining murine splenocytes qualitatively for mRNA for interleukin-2 (IL-2), IL-4, IL-10, IL-12p40, and gamma interferon (IFN-gamma), (ii) quantitating splenocyte mRNA for IL-12p40 by quantitative-competitive reverse transcriptase-mediated PCR, and (iii) measuring serum levels of IL-12p40 and IL-12p70 by capture enzyme-linked immunosorbent assay, each performed at selected intervals over 96 h after giving MAN. Further, the effect of in vivo administration of anti-IL-4 on the induction and elicitation of MAN-specific DH in MAN-treated mice was measured. Expression of IL-12p40 mRNA in the spleen was reduced to near 0 during the first 24 h but rebounded thereafter. Transcripts for IL-10 were present throughout the 96-h period, whereas those for IL-4 and IFN-gamma were either weak or undetectable prior to 24 to 48 h. In vivo administration of anti-IL-4 partially abrogated the downregulatory effect of MAN only when given at the time of MAN administration. Serum levels of IL-12p40, but not IL-12p70, were increased by 24 h and maximal at 48 h. The antagonistic effect of IL-12p40 could contribute to the mechanism(s) for downregulation of DH. Moreover, IL-10, IL-4, and/or IFN-gamma, interacting with MAN-activated cells in the absence of biologically active IL-12, may induce the production of CD8+ downregulatory effector cells. Partial abrogation of downregulatory activity in animals treated with anti-IL-4 at the time of induction of such activity lends support to this hypothesis.
给小鼠静脉注射白色念珠菌甘露糖蛋白(MAN)可刺激脾脏CD8 +效应细胞的产生,这些细胞会下调免疫小鼠的迟发型超敏反应(DH)。通过以下方式研究细胞因子在下调反应的诱导和/或引发中的作用:(i)定性检测小鼠脾细胞中白细胞介素-2(IL-2)、IL-4、IL-10、IL-12p40和γ干扰素(IFN-γ)的mRNA;(ii)通过定量竞争逆转录酶介导的PCR定量检测脾细胞中IL-12p40的mRNA;(iii)通过捕获酶联免疫吸附测定法测量给予MAN后96小时内选定时间间隔的血清IL-12p40和IL-12p70水平。此外,还测量了体内给予抗IL-4对经MAN处理的小鼠中MAN特异性DH的诱导和引发的影响。脾脏中IL-12p40 mRNA的表达在最初24小时内降至接近0,但此后反弹。IL-10的转录本在整个96小时期间都存在,而IL-4和IFN-γ的转录本在24至48小时之前要么很弱要么无法检测到。仅在给予MAN时给予抗IL-4,体内给予抗IL-4会部分消除MAN的下调作用。IL-12p40的血清水平在24小时时升高,并在48小时时达到最大值,而IL-12p70则没有。IL-12p40的拮抗作用可能有助于DH下调的机制。此外,在没有生物活性IL-12的情况下,IL-10、IL-4和/或IFN-γ与MAN激活的细胞相互作用,可能会诱导CD8 +下调效应细胞的产生。在诱导这种活性时用抗IL-4处理的动物中下调活性的部分消除支持了这一假设。