Obligately intracytosolic rickettsiae that cycle between arthropod and vertebrate hosts cause human diseases with a spectrum of severity, primarily by targeting microvascular endothelial cells, resulting in endothelial dysfunction. Endothelial cells and mononuclear phagocytes have important roles in the intracellular killing of rickettsiae upon activation by the effector molecules of innate and adaptive immunity. In overwhelming infection, immunosuppressive effects contribute to the severity of illness. Rickettsia-host cell interactions involve host cell receptors for rickettsial ligands that mediate cell adhesion and, in some instances, trigger induced phagocytosis. Rickettsiae interact with host cell actin to effect both cellular entry and intracellular actin-based mobility. The interaction of rickettsiae with the host cell also involves rickettsial evasion of host defense mechanisms and exploitation of the intracellular environment. Signal transduction events exemplify these effects. An intriguing frontier is the array of rickettsial noncoding RNA molecules and their potential effects on the pathogenesis and transmission of rickettsial diseases.

中文翻译：

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Ri病的发病机理：内生性感染的致病机制和免疫机制。

节肢动物和脊椎动物宿主之间循环的胞质立克次体主要通过靶向微血管内皮细胞而导致严重程度范围的人类疾病，从而导致内皮功能障碍。内皮细胞和单核吞噬细胞在先天性和适应性免疫效应分子激活后在立克次体的细胞内杀伤中起重要作用。在压倒性感染中，免疫抑制作用会加剧疾病的严重性。立克次体与宿主细胞的相互作用涉及立克次体配体的宿主细胞受体，这些受体介导细胞粘附并在某些情况下触发诱导的吞噬作用。立克次体与宿主细胞肌动蛋白相互作用，以影响细胞进入和基于细胞内肌动蛋白的迁移。立克次体与宿主细胞的相互作用还涉及立克次体逃避宿主防御机制和对细胞内环境的利用。信号转导事件例证了这些作用。有趣的前沿是立克次非编码RNA分子的阵列及其对立克次疾病的发病机理和传播的潜在影响。