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系统性红斑狼疮皮肤损伤的发病机制。

Pathogenesis of Skin Injury of Systemic Lupus Erythematosus.

机构信息

Key Laboratory of antibody techniques of ministry of health, Nanjing Medical University, Nanjing, China.

出版信息

Curr Rheumatol Rep. 2018 Feb 21;20(2):5. doi: 10.1007/s11926-018-0713-9.

Abstract

PURPOSE OF REVIEW

The second most common clinical expression in lupus patients is skin damage that the pathogenesis remains unclear. We discuss the role of pathological factors in the development of skin damage in SLE.

RECENT FINDINGS

Skin deposited IgG is a crucial pathologic factor in the development of skin damage in SLE. Macrophages and signaling of TNFα/TNFR1 and IFN/IFNR play an important role in the skin injury of SLE. The intracellular molecules including Syk and calcium/calmodulin 4 and NFAT are involved in the manifestation of skin damage in lupus-prone mice. UV is the most typical environmental factor to trigger skin injury in areas of IgG deposition in SLE. These evidences indicate that skin deposited IgG is a crucial pathological factor to trigger skin lesions in SLE and blockade of IgG signaling may be effective target against skin injury of SLE.

摘要

目的综述

狼疮患者的第二种最常见临床表现是皮肤损伤,但发病机制尚不清楚。我们讨论了病理因素在 SLE 皮肤损伤发展中的作用。

最近的发现

皮肤沉积 IgG 是 SLE 皮肤损伤发展中的关键病理因素。巨噬细胞和 TNFα/TNFR1 及 IFN/IFNR 的信号转导在 SLE 的皮肤损伤中起着重要作用。细胞内分子包括 Syk 和钙/钙调蛋白 4 和 NFAT 参与狼疮易感小鼠的皮肤损伤表现。紫外线是触发 SLE 中 IgG 沉积部位皮肤损伤的最典型环境因素。这些证据表明,皮肤沉积 IgG 是触发 SLE 皮肤病变的关键病理因素,阻断 IgG 信号可能是治疗 SLE 皮肤损伤的有效靶点。

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