Williams J, Johnson S, Mascali J J, Smith H, Rosenwasser L J, Borish L
Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.
J Immunol. 1992 Oct 15;149(8):2823-9.
Mononuclear phagocytic cells contain low affinity receptors for IgE (Fc epsilon RII or CD23) which induce cellular activation in the presence of specific allergen. These studies were performed to quantify the expression by monocytes and alveolar macrophages of Fc epsilon RII in asthma and to determine biologic response modifiers that regulate Fc epsilon RII. Whereas 2.5 +/- 1.0% of the monocytes obtained from normal volunteers were Fc epsilon RII positive, this increased to 16.7 +/- 2.4% in asthma (p < 0.001). Stimulation of Fc epsilon RII expression on monocytes was shown to be an activity of IL-4 (24.5 +/- 5.9%), granulocyte-macrophage-CSF (28.1 +/- 5.2%), IFN-alpha (15.8 +/- 5.3%), IFN-gamma (10.4 +/- 3.7%), and macrophage-CSF (7.3 +/- 0.7%) but not of IL-2, IL-6, or TNF-alpha. Expression of Fc epsilon RII by these cytokines was associated with the induction of specific mRNA transcripts. Using Fc epsilon RII subtype specific primers in the polymerase chain reaction expansion of cDNA, cytokine-induced receptors were shown to be Fc epsilon RIIb. Alveolar macrophages from nonasthmatic subjects displayed minimal expression of Fc epsilon RII (3.2 +/- 1.2%); however, these receptors were present on 69.2 +/- 6.3% of asthmatic volunteers (p < 0.001). Induction of Fc epsilon RII appears specific for allergic asthma insofar as these receptors are also not expressed in subjects with interstitial lung disease (1.3 +/- 1.3%). As assessed by shift in mean fluorescence, instillation of allergen in the asthmatic's airway further up-regulated Fc epsilon RII on alveolar macrophages by 151 +/- 7%. Up-regulation of Fc epsilon RII in atopic individuals may therefore reflect allergen-induced exposure of mononuclear phagocytes to one or more of these cytokines. These studies suggest a mechanism by which an immunologic stimulus that leads to the production of these cytokines (e.g., allergen or viral infection) would contribute to the development or exacerbation of allergic disease.
单核吞噬细胞含有IgE的低亲和力受体（FcεRII或CD23），在存在特异性变应原的情况下可诱导细胞活化。进行这些研究的目的是量化哮喘患者单核细胞和肺泡巨噬细胞中FcεRII的表达，并确定调节FcεRII的生物反应调节剂。从正常志愿者获得的单核细胞中，2.5±1.0%为FcεRII阳性，而在哮喘患者中这一比例增加到16.7±2.4%（p<0.001）。单核细胞上FcεRII表达的刺激被证明是IL-4（24.5±5.9%）、粒细胞-巨噬细胞集落刺激因子（28.1±5.2%）、IFN-α（15.8±5.3%）、IFN-γ（10.4±3.7%）和巨噬细胞集落刺激因子（7.3±0.7%）的活性，但不是IL-2、IL-6或TNF-α的活性。这些细胞因子诱导的FcεRII表达与特异性mRNA转录本的诱导相关。在cDNA的聚合酶链反应扩增中使用FcεRII亚型特异性引物，细胞因子诱导的受体显示为FcεRIIb。非哮喘受试者的肺泡巨噬细胞FcεRII表达极少（3.2±1.2%）；然而，这些受体存在于69.2±6.3%的哮喘志愿者中（p<0.001）。FcεRII的诱导似乎对过敏性哮喘具有特异性，因为这些受体在间质性肺病患者中也不表达（1.3±1.3%）。通过平均荧光的变化评估，在哮喘患者气道中滴注变应原可使肺泡巨噬细胞上的FcεRII进一步上调151±7%。因此，特应性个体中FcεRII的上调可能反映变应原诱导单核吞噬细胞暴露于这些细胞因子中的一种或多种。这些研究提示了一种机制，通过该机制导致这些细胞因子产生的免疫刺激（如变应原或病毒感染）会促进过敏性疾病的发生或加重。
