Nihei Y, Maruyama K, Zhang J Z, Kobayashi K, Kaneko F
Department of Dermatology, Fukushima Medical College, Japan.
Arch Dermatol Res. 1995;287(6):546-52. doi: 10.1007/BF00374074.
Secretory component (SC) acts as a transmembrane polymeric immunoglobulin receptor of epithelial cells and is known to bind to polymeric IgA and to contribute to the secretion of secretory IgA (sIgA). We describe a new biological function for free SC (FSC) by which the expression of intercellular adhesion molecule-1 (ICAM-1) and HLA-DR induced by interferon gamma (IFN gamma) is inhibited in human keratinocytes. This activity coincided with suppression of adenosine cyclic 3,5-monophosphate (cyclic AMP) production in keratinocytes. Keratinocytes produced SC after stimulation with IFN gamma and this production was suppressed by the addition of H-7 or propranolol. The addition of propranolol resulted in prolongation of ICAM-1 expression on keratinocytes induced by IFN gamma. These results suggest that endogenously produced SC, as well as exogenously added FSC, acts as an inhibitor of IFN gamma. Therefore, our results suggest that SC plays an antiinflammatory role in the pathogenesis of inflammatory skin diseases via inhibition in keratinocytes of IFN gamma induced expression of ICAM-1 and HLA-DR.
分泌成分（SC）作为上皮细胞的跨膜多聚免疫球蛋白受体，已知其可与多聚IgA结合并有助于分泌型IgA（sIgA）的分泌。我们描述了游离SC（FSC）的一种新生物学功能，即FSC可抑制人角质形成细胞中由干扰素γ（IFNγ）诱导的细胞间黏附分子-1（ICAM-1）和HLA-DR的表达。该活性与角质形成细胞中3,5-环磷酸腺苷（环磷酸腺苷）生成的抑制相一致。角质形成细胞在受到IFNγ刺激后产生SC，而H-7或普萘洛尔的添加可抑制这种产生。普萘洛尔的添加导致IFNγ诱导的角质形成细胞上ICAM-1表达的延长。这些结果表明，内源性产生的SC以及外源性添加的FSC均作为IFNγ的抑制剂发挥作用。因此，我们的结果表明，SC通过抑制角质形成细胞中IFNγ诱导的ICAM-1和HLA-DR的表达，在炎症性皮肤病的发病机制中发挥抗炎作用。
