Chtanova Tatyana, Han Seong-Ji, Schaeffer Marie, van Dooren Giel G, Herzmark Paul, Striepen Boris, Robey Ellen A
Department of Molecular and Cell Biology, Life Sciences Addition, University of California, Berkeley, CA 94720, USA.
Immunity. 2009 Aug 21;31(2):342-55. doi: 10.1016/j.immuni.2009.06.023.
Memory T cells circulate through lymph nodes where they are poised to respond rapidly upon re-exposure to a pathogen; however, the dynamics of memory T cell, antigen-presenting cell, and pathogen interactions during recall responses are largely unknown. We used a mouse model of infection with the intracellular protozoan parasite, Toxoplasma gondii, in conjunction with two-photon microscopy, to address this question. After challenge, memory T cells migrated more rapidly than naive T cells, relocalized toward the subcapsular sinus (SCS) near invaded macrophages, and engaged in prolonged interactions with infected cells. Parasite invasion of T cells occurred by direct transfer of the parasite from the target cell into the T cell and corresponded to an antigen-specific increase in the rate of T cell invasion. Our results provide insight into cellular interactions during recall responses and suggest a mechanism of pathogen subversion of the immune response.
记忆T细胞在淋巴结中循环,随时准备在再次接触病原体时迅速做出反应;然而,在回忆反应期间记忆T细胞、抗原呈递细胞和病原体相互作用的动态过程在很大程度上尚不清楚。我们使用细胞内原生动物寄生虫刚地弓形虫感染的小鼠模型,并结合双光子显微镜来解决这个问题。受到攻击后,记忆T细胞比初始T细胞迁移得更快,重新定位到被入侵巨噬细胞附近的被膜下窦(SCS),并与受感染细胞进行长时间的相互作用。寄生虫通过从靶细胞直接转移到T细胞而侵入T细胞,这与T细胞侵入率的抗原特异性增加相对应。我们的结果为回忆反应期间的细胞相互作用提供了见解,并提出了病原体颠覆免疫反应的一种机制。