Detection of a gamma interferon-induced protein IP-10 in psoriatic plaques.

Detection of a gamma interferon-induced protein IP-10 in psoriatic plaques.
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DOI:
10.1084/jem.168.3.941
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发表时间:
1988-09-01
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
Carter DM
Carter DM
中科院分区:
其他
文献类型:
--
作者:
Gottlieb AB;Luster AD;Posnett DN;Carter DM

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银屑病斑块的病理特征是炎症和表皮更新增加。 IP-10 是一种由γ-干扰素诱导表达的细胞因子,是具有炎症和生长促进活性的可溶性介质家族的成员。在免疫过氧化物酶研究中,使用亲和纯化的兔抗 IP-10 抗体在角质形成细胞和活动性银屑病斑块的真皮浸润中检测到 IP-10 蛋白。成功治疗活性斑块可降低斑块中 IP-10 的表达。使用 IP-10 cDNA 探针进行 Northern 印迹分析证实了这些结果。我们之前在活动性银屑病斑块中检测到活化的 T 细胞和 HLA-DR 角质形成细胞。由于 IP-10 在延迟的细胞免疫反应中被检测到,本研究进一步指出了持续的细胞免疫反应在银屑病发病机制中的作用。
The pathologic features of psoriatic plaques are inflammation and increased epidermal turnover. IP-10, a cytokine the expression of which is induced by gamma-interferon, is a member of a family of soluble mediators with inflammatory and growth-promoting activities. IP-10 protein was detected in keratinocytes and the dermal infiltrate from active psoriatic plaques using an affinity-purified rabbit anti-IP-10 antibody in immunoperoxidase studies. Successful treatment of active plaques decreased IP-10 expression in plaques. These results were corroborated by Northern blot analysis with an IP-10 cDNA probe. We have previously detected activated T cells and HLA-DR keratinocytes in active psoriatic plaques. Since IP-10 is detected in delayed cellular immune responses, the present study further points to the role of ongoing cellular immune responses in the pathogenesis of psoriasis.