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Pathogenesis of B-Cell Superantigen-Induced Immune Complex-Mediated Inflammation

机译：B细胞超抗原诱导的免疫复合物介导的炎症的发病机理。

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Staphylococcal protein A (SpA) is representative of a new class of antigens, the B-cell superantigens (SAgs). These antigens bind to the Fab regions of immunoglobulin molecules outside their complementarity-determining regions. SpA, the best-studied B-cell SAg, reacts with the Fabs of most VH3+ immunoglobulins, which are expressed on 30 to 60% of human peripheral B cells. Therefore, B-cell SAgs like SpA have great potential to elicit inflammatory responses in vivo. We previously reported that the interaction of SpA with VH3+ immunoglobulin molecules leads to activation of the complement cascade and produces a histologic pattern of inflammation in the skin of a rabbit indicative of immune complex injury. To elucidate the cellular and molecular events contributing to this type of unconventional immune complex-mediated inflammation, we established a mouse peritoneal Arthus reaction model. Mice treated intravenously with human polyclonal immunoglobulin G (IgG), followed by intraperitoneal injection of SpA, showed neutrophil influx into the peritoneal cavity with peak numbers appearing at 8 h. This inflammatory reaction was dependent on the interaction of SpA with VH3+ IgG. Mast cells, FcγRIII, complement components, and tumor necrosis factor alpha play obligatory roles, and the reaction is associated with the local release of the CXC chemokines macrophage inflammatory protein 2 and KC. The data provide further compelling evidence for the induction of immune complex-mediated injury by a B-cell SAg and highlight important factors contributing to the pathogenesis of this novel type of inflammatory reaction.
机译：葡萄球菌蛋白A（SpA）代表了一类新的抗原，即B细胞超抗原（SAgs）。这些抗原在其互补决定区之外结合免疫球蛋白分子的Fab区。 SpA是研究最深入的B细胞SAg，可与大多数V H 3 + 免疫球蛋白的Fab反应，并在30％至60％的人类外周血B细胞中表达。因此，像SpA一样的B细胞SAg在体内具有引发炎症反应的巨大潜力。我们先前曾报道SpA与V H 3 + 免疫球蛋白分子的相互作用导致补体级联反应的激活，并在兔皮肤中产生炎症的组织学模式，这表明免疫复合物损伤。为了阐明导致这种类型的非常规免疫复合物介导的炎症的细胞和分子事件，我们建立了小鼠腹膜Arthus反应模型。用人多克隆免疫球蛋白G（IgG）静脉内治疗，然后腹膜内注射SpA的小鼠显示嗜中性粒细胞流入腹膜腔，在8 h出现峰值。这种炎症反应取决于SpA与V H 3 + IgG的相互作用。肥大细胞，FcγRIII，补体成分和肿瘤坏死因子α起强制性作用，并且该反应与CXC趋化因子巨噬细胞炎性蛋白2和KC的局部释放有关。该数据为由B细胞SAg诱导免疫复合物介导的损伤提供了进一步的令人信服的证据，并突出了促成这种新型炎症反应的发病机理的重要因素。

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