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首页> 外文期刊>Nature clinical practice. Rheumatology >Mechanisms of disease: a 'DAMP' view of inflammatory arthritis.
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Mechanisms of disease: a 'DAMP' view of inflammatory arthritis.

机译：疾病机理：炎性关节炎的“ DAMP”观点。

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Innate immunity achieves our primary host defense by recognizing invading microorganisms through pathogen-associated molecular patterns (PAMPs) and by reacting to tissue damage signals called damage-associated molecular patterns (DAMPs). DAMP molecules, including high mobility group box 1 protein (HMGB-1), heat-shock proteins (HSPs), uric acid, altered matrix proteins, and S100 proteins, represent important danger signals that mediate inflammatory responses through the receptor for advanced glycation end-products (RAGE, also known as AGER) and Toll-like receptors, after release from activated or necrotic cells. The terms 'alarmins' and 'endokines' have also been proposed for DAMP molecules. A prototypic DAMP molecule, the nuclear protein HMGB-1, is either passively released by necrotic cells or actively secreted with delay by activated cells. S100A8, S100A9, and S100A12 are calcium-binding proteins expressed in the cytoplasm of phagocytes. They are rapidly secreted by activated monocytes or neutrophils, which are abundant in inflamed synovial tissue. HSPs are involved in the crosstalk between innate and adaptive immune systems, and primarily mediate immune regulatory functions. Multiple positive feedback loops between DAMPs and PAMPs and their overlapping receptors temporally and spatially drive these processes and may represent the molecular basis for the observation that infections, as well as nonspecific stress factors, can trigger flares in rheumatic diseases.
机译：先天性免疫通过识别病原体相关分子模式（PAMP）入侵的微生物并与称为损伤相关分子模式（DAMP）的组织损伤信号发生反应，从而实现了我们的主要宿主防御能力。 DAMP分子，包括高迁移率第1族盒蛋白（HMGB-1），热休克蛋白（HSP），尿酸，改变的基质蛋白和S100蛋白，代表着重要的危险信号，这些信号通过受体进入晚期糖基化末端来介导炎症反应从活化或坏死细胞释放后的副产物（RAGE，也称为AGER）和Toll样受体。对于DAMP分子也已经提出了术语“ alarmins”和“ endokines”。原型DAMP分子，核蛋白HMGB-1，可以由坏死细胞被动释放，也可以由活化细胞延迟主动分泌。 S100A8，S100A9和S100A12是在吞噬细胞的细胞质中表达的钙结合蛋白。它们被活化的单核细胞或嗜中性粒细胞迅速分泌，它们在发炎的滑膜组织中丰富。 HSP参与先天性和适应性免疫系统之间的串扰，并且主要介导免疫调节功能。 DAMPs和PAMPs及其重叠的受体之间的多个正反馈回路在时间和空间上驱动着这些过程，并且可能代表了观察到感染以及非特异性应激因素会触发风湿性疾病发作的分子基础。

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