MONOCYTES AND POLYMORPHONUCLEAR NEUTROPHILS OF PATIENTS WITH STREPTOCOCCAL PHARYNGITIS EXPRESS INCREASED NUMBERS OF TYPE-I IGG FC-RECEPTORS
MONOCYTES AND POLYMORPHONUCLEAR NEUTROPHILS OF PATIENTS WITH STREPTOCOCCAL PHARYNGITIS EXPRESS INCREASED NUMBERS OF TYPE-I IGG FC-RECEPTORS
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DOI：
10.1172/jci114921
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发表时间：
1990-12-01
影响因子：
15.9
通讯作者：
FANGER, MW
中科院分区：
文献类型：
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作者：
GUYRE, PM;CAMPBELL, AS;FANGER, MW
使用培养细胞的研究已经表明，γ干扰素（IFN-γ）诱导Fc γ RI（IgG的I型Fc受体）在人多形核中性粒细胞（PMN）上的表达，并大大增加人单核细胞上这些受体的数量。rIFN-γ的施用也导致这些细胞群上Fc γ RI表达增强。因为链球菌抗原是IFN-γ的有效诱导剂。在体外，我们假设IFN-γ。会在链球菌感染的患者体内内源性产生。这种IFN-γ的产生在体内，即使在低水平，也可以预期诱导Fc γ RI在单核细胞和嗜中性粒细胞上的表达。为了评估这种可能性，我们使用对Fc γ RI特异的单克隆抗体32（mAb 32）来定量人外周血细胞上该受体的表达。我们测量了mAb 32与分离自健康供体和A β-MG患者的单核细胞和PMN的结合。溶血性链球菌（GABHS）咽炎。来自健康供体的PMN（n = 12）具有700 ± 0.001 μ g/ml的浓度。600（平均值±）SD）mAb 32结合位点。GABHS咽喉培养阴性的咽炎患者（n = 11）有2，100 ±。1,600个网站在他们的PMNs上。相比之下，来自患有记录的GABHS咽炎的患者（n = 12）的PMN具有11，600 ± 0.5%。7，500个mAb 32结合位点。Fc γ RI在单核细胞上的表达也有类似的变化，对照单核细胞的平均值为19，900 ± 0.05。每个细胞有3，200个mAb 32个结合位点，GABHS阳性单核细胞有47，500个。21，400个站点。GABHS阴性咽喉培养物组具有略微升高的Fc γ RI数量，平均值为28，200 ±。8,400个站点。10名有记录的尿路感染患者和3名无并发症的肾盂肾炎患者的Fc γ RI表达没有升高。这些研究表明，局部A组链球菌感染可引起整个吞噬细胞循环池的全身激活，并表明类似水平的激活在局部革兰氏阴性尿路感染中是罕见的。
Studies using cultured cells have shown that gamma interferon (IFN-.gamma.) induces the expression of Fc.gamma.RI (the type I Fc receptor for IgG) on human polymorphonuclear neutrophils (PMN) and greatly increases the number of these receptors on human monocytes. Administration of rIFN-.gamma. in vivo also causes enhanced Fc.gamma.RI expression on these cell populations. Because streptococcal antigens are potent inducers of IFn-.gamma. in vitro, we postulated that IFN-.gamma. would be produced endogenously in vivo in patients with streptococcal infections. Such production of IFN-.gamma. in vivo, even at low levels, might be expected to induce the expression of Fc.gamma.RI on monocytes and neutrophils. To evaluate this possibility, we used monoclonal antibody 32 (mAb 32), which is specific for Fc.gamma.RI, to quantitate the expression of this receptor on human peripheral blood cells. We measured the binding of mAb 32 to monocytes and PMNs isolated from healthy donors and from patients with group A .beta.-hemolytic streptococcal (GABHS) pharyngitis. PMNs from healthy donors (n = 12) had 700 .+-. 600 (mean .+-. SD) mAb 32 binding sites. Patients with pharyngitis and negative throat culture for GABHS (n = 11) had 2,100 .+-. 1,600 sites on their PMNs. In contrast, the PMNs from patients with documented GABHS pharyngitis (n = 12) had 11,600 .+-. 7,500 mAb 32 binding sites on their surface. There was a similar change in the expression of Fc.gamma.RI on monocytes, with control monocytes having a mean of 19,900 .+-. 3,200 mAb 32 binding sites per cell and the GABHS-positive monocytes having 47,500 .+-. 21,400 sites. The GABHS-negative throat culture group had a slightly elevated number of Fc.gamma.RI with a mean of 28,200 .+-. 8,400 sites. 10 patients with documented urinary tract infections and three patients with uncomplicated pyelonephritis had no elevation in Fc.gamma.RI expression. These studies demonstrate that a localized group A streptococcal infection can cause systemic activation of the entire circulating pool of phagocytes, and suggest that a similar level of activation is uncommon in localized gram-nagative infections of the urinary tract.