PDF(Pubmed)
Abstract：
The mechanisms underlying the onset and progression of vasculitis remain poorly understood. This condition is characterized by damage to the vascular wall, recruitment of inflammatory cells, and subsequent structural remodeling, which are hallmarks of vasculitis. The histopathological classification of vasculitis relies on the size of the affected vessel and the predominant type of inflammatory cell involved - neutrophils in acute cases, lymphocytes in chronic conditions, and histiocytes in granulomatous forms. Pathological changes progress in every context, and a single vasculitic pattern can be associated with various systemic conditions. Conversely, a single causative agent may lead to multiple distinct clinical and pathological manifestations of vasculitis. Moreover, many cases of vasculitis have no identifiable cause. A foundational understanding of the normal structure of the cutaneous vascular network is crucial. Similarly, identifying the cellular and molecular participants and their roles in forming the \"dermal microvascular unit\" is propedeutical.
This review aims to elucidate the complex mechanisms involved in the initiation and progression of vasculitis, offering a comprehensive overview of its histopathological classification, underlying causes, and the significant role of the cutaneous vascular network and cellular dynamics. By integrating the latest insights from studies on NETosis and the implications of lymphocytic infiltration in autoimmune diseases, we seek to bridge gaps in current knowledge and highlight areas for future research. Our discussion extends to the clinical implications of vasculitis, emphasizing the importance of identifying etiological agents and understanding the diverse histopathological manifestations to improve diagnostic accuracy and treatment outcomes.
This review aims to elucidate the complex mechanisms involved in the initiation and progression of vasculitis, offering a comprehensive overview of its histopathological classification, underlying causes, and the significant role of the cutaneous vascular network and cellular dynamics. By integrating the latest insights from studies on NETosis and the implications of lymphocytic infiltration in autoimmune diseases, we seek to bridge gaps in current knowledge and highlight areas for future research. Our discussion extends to the clinical implications of vasculitis, emphasizing the importance of identifying etiological agents and understanding the diverse histopathological manifestations to improve diagnostic accuracy and treatment outcomes.
摘要：
血管炎的发病和进展的潜在机制仍然知之甚少。这种情况的特征是血管壁受损，炎症细胞的募集，以及随后的结构重塑，这是血管炎的标志。血管炎的组织病理学分类取决于受影响血管的大小和所涉及的主要类型的炎症细胞-急性病例中的中性粒细胞，慢性淋巴细胞，和肉芽肿形式的组织细胞。病理变化在各种情况下都在进步，和单一的血管模式可以与各种全身状况有关。相反，单一病原体可能导致血管炎的多种不同的临床和病理表现。此外，许多血管炎病例没有明确的病因。对皮肤血管网的正常结构的基本理解至关重要。同样，确定细胞和分子参与者及其在形成“真皮微血管单元”中的作用是有前景的。
这篇综述旨在阐明血管炎发生和进展的复杂机制，提供其组织病理学分类的全面概述，根本原因，以及皮肤血管网络和细胞动力学的重要作用。通过整合NETosis研究的最新见解和淋巴细胞浸润在自身免疫性疾病中的意义，我们寻求弥合当前知识的差距，并突出未来研究的领域。我们的讨论延伸到血管炎的临床意义，强调确定病因和了解不同的组织病理学表现的重要性，以提高诊断准确性和治疗结果。
这篇综述旨在阐明血管炎发生和进展的复杂机制，提供其组织病理学分类的全面概述，根本原因，以及皮肤血管网络和细胞动力学的重要作用。通过整合NETosis研究的最新见解和淋巴细胞浸润在自身免疫性疾病中的意义，我们寻求弥合当前知识的差距，并突出未来研究的领域。我们的讨论延伸到血管炎的临床意义，强调确定病因和了解不同的组织病理学表现的重要性，以提高诊断准确性和治疗结果。
