Zhao Yanlin, Reyes Jojo, Rovira-Diaz Eliezer, Fox Barbara A, Bzik David J, Yap George S
Department of Medicine and Center for Immunity and Inflammation, New Jersey Medical School, Rutgers University, Newark, NJ; and.
Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, NH.
J Immunol. 2021 Sep 15;207(6):1507-1512. doi: 10.4049/jimmunol.2100605. Epub 2021 Aug 16.
Resistance and tolerance are vital for survivability of the host-pathogen relationship. Virulence during infection in mice is mediated by parasite kinase-dependent antagonism of IFN-γ-induced host resistance. Whether avirulence requires expression of parasite factors that induce host tolerance mechanisms or is a default status reflecting the absence of resistance-interfering factors is not known. In this study, we present evidence that avirulence in requires parasite engagement of the scavenger receptor CD36. CD36 promotes macrophage tropism but is dispensable for the development of resistance mechanisms. Instead CD36 is critical for re-establishing tissue homeostasis and survival following the acute phase of infection. The CD36-binding capacity of strains is negatively controlled by the virulence factor, ROP18. Thus, the absence of resistance-interfering virulence factors and the presence of tolerance-inducing avirulence factors are both required for long-term host-pathogen survival.
抗性和耐受性对于宿主 - 病原体关系的生存能力至关重要。小鼠感染期间的毒力由寄生虫激酶依赖性拮抗IFN - γ诱导的宿主抗性介导。无毒力是需要诱导宿主耐受机制的寄生虫因子表达，还是反映缺乏抗性干扰因子的默认状态尚不清楚。在本研究中，我们提供证据表明，无毒力需要寄生虫与清道夫受体CD36结合。CD36促进巨噬细胞嗜性，但对于抗性机制的发展并非必需。相反，CD36对于感染急性期后重建组织稳态和生存至关重要。菌株的CD36结合能力受毒力因子ROP18的负调控。因此，长期宿主 - 病原体生存既需要缺乏抗性干扰毒力因子，也需要存在诱导耐受性的无毒力因子。
