Mahanty S, Ravichandran M, Raman U, Jayaraman K, Kumaraswami V, Nutman T B
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Infect Immun. 1997 May;65(5):1742-7. doi: 10.1128/iai.65.5.1742-1747.1997.
We investigated the mechanisms by which interleukin-10 (IL-10) regulates antigen-specific hyporesponsiveness in asymptomatic microfilaremic (MF) individuals. Peripheral blood mononuclear cells from MF individuals (n = 11) were stimulated in vitro with Brugia malayi antigen (BMA) or mycobacterial purified protein derivative (PPD) in the presence of neutralizing anti-IL-10 or isotype control monoclonal antibodies. As expected, BMA stimulated little or no gamma interferon (IFN-gamma) secretion in MF individuals, whereas PPD stimulated IFN-gamma in all but one. Neutralization of endogenous BMA-driven IL-10 secretion led to augmentation of IFN-gamma in seven of nine MF individuals (1.5- to 10-fold) and did so in a BMA-specific manner (PPD-driven IFN-gamma was augmented in only two of eight MF individuals and only 1.5- to 2-fold), indicating that IL-10 downregulates type 1 responses in these individuals. Type 2 responses (IL-5 secretion) were unaffected by the IL-10 blockade. To assess whether IL-12 could reverse the type 1 downregulation observed, the effect of recombinant human IL-12 (rhIL-12) on BMA-driven IL-5 and IFN-gamma production was also evaluated. rhIL-12 augmented both BMA- and PPD-driven IFN-gamma production 5- to 10-fold in six of nine MF individuals. These data demonstrate that IL-10 downregulates BMA-driven type 1 responses and that IL-12 can overcome downregulation of Th1 responses associated with MF but does so in a non-antigen-specific manner.
我们研究了白细胞介素-10(IL-10)调节无症状微丝蚴血症(MF)个体抗原特异性低反应性的机制。在存在中和性抗IL-10或同型对照单克隆抗体的情况下,用马来布鲁线虫抗原(BMA)或结核分枝杆菌纯化蛋白衍生物(PPD)体外刺激MF个体(n = 11)的外周血单个核细胞。正如预期的那样,BMA刺激MF个体产生很少或不产生γ干扰素(IFN-γ),而PPD刺激除一人外的所有个体产生IFN-γ。内源性BMA驱动的IL-10分泌的中和导致9名MF个体中的7名(1.5至10倍)IFN-γ增加,并且以BMA特异性方式增加(PPD驱动的IFN-γ仅在8名MF个体中的2名中增加,仅1.5至2倍),表明IL-10下调这些个体中的1型反应。2型反应(IL-5分泌)不受IL-10阻断的影响。为了评估IL-12是否可以逆转观察到的1型下调,还评估了重组人IL-12(rhIL-12)对BMA驱动的IL-5和IFN-γ产生的影响。rhIL-12使9名MF个体中的6名中BMA和PPD驱动的IFN-γ产生增加5至10倍。这些数据表明,IL-10下调BMA驱动的1型反应,并且IL-12可以克服与MF相关的Th1反应的下调,但以非抗原特异性方式进行。