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前列腺自身免疫:从实验模型到临床对应物。

Prostate autoimmunity: from experimental models to clinical counterparts.

机构信息

Intercept Pharmaceuticals, 06073 Corciano (Perugia), Italy.

出版信息

Expert Rev Clin Immunol. 2009 Sep;5(5):577-86. doi: 10.1586/eci.09.37.

Abstract

Different murine models of autoimmune prostatitis have been developed and characterized, proving the autoimmune origin of this pathology. Autoimmune prostatitis models have also provided a wealth of information on the mechanisms involved in disease development, shedding light on inciting autoantigens, regulatory and pathogenic T cells, and mediators of prostatic autoimmunity. Unfortunately, the clinical counterparts of experimental autoimmune prostatitis are still poorly defined. In this review, we will discuss evidence for the autoimmune origin of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and the chronic inflammatory nature of benign prostatic hyperplasia (BPH). The autoimmune pathogenesis of CP/CPPS and the chronic inflammation characteristic of BPH will be reviewed within the context of the recent demonstration that human prostate stromal cells from BPH tissue can act as antigen-presenting cells and are not only able to activate CD4(+) T lymphocytes, but can also produce IL-12 and IL-23, which are key cytokines for the induction of pathogenic Th1 and Th17 cells.

摘要

已经开发和表征了不同的自身免疫性前列腺炎的小鼠模型,证明了这种病理学的自身免疫起源。自身免疫性前列腺炎模型还提供了大量关于疾病发展所涉及的机制的信息,揭示了引发自身抗原、调节性和致病性 T 细胞以及前列腺自身免疫的介质。不幸的是,实验性自身免疫性前列腺炎的临床对应物仍未明确定义。在这篇综述中,我们将讨论慢性前列腺炎/慢性骨盆疼痛综合征 (CP/CPPS) 的自身免疫起源和良性前列腺增生 (BPH) 的慢性炎症性质的证据。将在最近证明 BPH 组织中的人类前列腺基质细胞可以作为抗原呈递细胞的背景下,综述 CP/CPPS 的自身免疫发病机制和 BPH 的慢性炎症特征,这些细胞不仅能够激活 CD4(+) T 淋巴细胞,还能够产生 IL-12 和 IL-23,这是诱导致病性 Th1 和 Th17 细胞的关键细胞因子。

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