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白塞病(阿达姆安泰斯-白塞病)。

Behçet's disease (Adamantiades-Behçet's disease).

作者信息

Kaneko Fumio, Togashi Ari, Saito Sanae, Sakuma Hideo, Oyama Noritaka, Nakamura Koichiro, Yokota Kenji, Oguma Keiji

机构信息

Institute of Dermato-Immunology and Allergy, Southern TOHOKU Research Institute for Neuroscience, 7-115 Yatsuyamada, Koriyama, Fukushima 963-8563, Japan.

出版信息

Clin Dev Immunol. 2011;2011:681956. doi: 10.1155/2011/681956. Epub 2010 Nov 1.

Abstract

Adamantiades-Behçet's disease (ABD) is characterized by starting with oral aphthous ulceration and developing of the systemic involvements. The pathogenesis of ABD is closely correlated with the genetic factors and the triggering factors which acquire delayed-type hypersensitivity reaction against oral streptococci mediated by IL-12 cytokine family. HLA-B51 is associated in more than 60% of the patients and its restricted CD8+ T cell response is clearly correlated with the target tissues. Bes-1 gene encoded partial S. sanguinis genome which is highly homologous with retinal protein, and 65 kD heat shock protein (Hsp-65) released from streptococci is playing an important role with human Hsp-60 in the pathogenesis of ABD. Although Hsp-65/60 has homologies with the respective T cell epitope, it stimulates peripheral blood mononuclear cells (PBMCs) from ABD patients. On the other hand, some peptides of Hsp-65 were found to reduce IL-8 and IL-12 production from PBMCs of ABD patients in active stage.

摘要

白塞病(ABD)的特征是始于口腔阿弗他溃疡并发展为全身受累。ABD的发病机制与遗传因素以及由IL-12细胞因子家族介导的针对口腔链球菌的迟发型超敏反应触发因素密切相关。超过60%的患者与HLA-B51相关,其受限的CD8 + T细胞反应与靶组织明显相关。Bes-1基因编码与视网膜蛋白高度同源的部分血链球菌基因组,链球菌释放的65kD热休克蛋白(Hsp-65)在ABD发病机制中与人类Hsp-60发挥重要作用。尽管Hsp-65/60与各自的T细胞表位具有同源性,但它能刺激ABD患者的外周血单核细胞(PBMC)。另一方面,发现Hsp-65的一些肽可减少活动期ABD患者PBMC中IL-8和IL-12的产生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7105/2967828/1d599dc405aa/CDI2011-681956.001.jpg

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