Protective immunity to Rickettsia tsutsugamushi in a murine model is dependent upon the development of cell mediated immunity, as demonstrated by lymphocyte transfer, production of lymphokines and -interferon by thymus-derived lymphocytes, activation of macrophages by lymphokines and demonstration of delayed-type hypersensitivity response following exposure to these organisms. Infection of mice with small numbers of Rickettsia typhi inoculated by a peripheral route leads to a more complex pattern of immune development, with a distinction between resistance to local and systemic infection. Nevertheless, thymus-derived lymphocytes and activated macrophages play a major role in modulating pathogenesis of infection, and delayed-type hypersensitivity responses are evident. Spotted fever group rickettsiae also elicit a cell-mediated response in rodents, and protection against Rickettsia conorii infection has been achieved by adoptive transfer of thymus-derived lymphocytes from immune animals. Limited studies with Rickettsia akari suggest that activation of mouse macrophages is critical to host survival following infection with this organism.
在鼠类模型中，对恙虫病立克次体的保护性免疫依赖于细胞介导免疫的发展，淋巴细胞转移、胸腺来源淋巴细胞产生淋巴因子和γ干扰素、淋巴因子激活巨噬细胞以及接触这些病原体后出现迟发型超敏反应均证明了这一点。经外周途径给小鼠接种少量伤寒立克次体后，会导致更复杂的免疫发展模式，对局部感染和全身感染的抵抗力有所不同。然而，胸腺来源淋巴细胞和活化巨噬细胞在调节感染发病机制中起主要作用，迟发型超敏反应也很明显。斑点热群立克次体在啮齿动物中也引发细胞介导反应，通过从免疫动物体内过继转移胸腺来源淋巴细胞已实现对康氏立克次体感染的保护。对小蛛立克次体的有限研究表明，小鼠巨噬细胞的激活对感染该病原体后的宿主存活至关重要。
