Guangdong Provincial Key Laboratory of Allergy and Clinical Immunology, The State Key Laboratory of Respiratory Disease, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
Front Immunol. 2019 Sep 13;10:2154. doi: 10.3389/fimmu.2019.02154. eCollection 2019.
CD4 T follicular helper (Tfh) cells, a new subset of immune cells, have been demonstrated to be involved in granulomatous responses to infection. However, the role and underlying mechanisms of Tfh cell aggregation in infection remain incompletely understood. In this study, we provide evidence that infection enhances the accumulation of Tfh cells in the spleen, lymph nodes, and peripheral blood of C57BL/6 mice. Infection-induced Tfh cells exhibited more potent effects directly on B cell responses than the control Tfh cells ( < 0.05). Furthermore, reduced apoptosis of Tfh cells was found both in infected mice and in soluble egg antigen (SEA) treated Tfh cells ( < 0.05). Mechanistic studies reveal that caspase-3 is the primary drivers of down-regulated apoptotic Tfh cell death in infection. In summary, this study demonstrates that Tfh cell accumulation might have an impact on the generation of immune responses in infection, and caspase-3 signaling mediated apoptosis down-regulation might responsible for the accumulation of Tfh cell in this course.
CD4+滤泡辅助性 T(Tfh)细胞是一种新型免疫细胞亚群,已被证明参与了感染后的肉芽肿反应。然而,Tfh 细胞在感染中的聚集作用及其潜在机制仍不完全清楚。本研究提供了证据表明,感染增强了 C57BL/6 小鼠脾脏、淋巴结和外周血中 Tfh 细胞的积累。感染诱导的 Tfh 细胞对 B 细胞反应的直接作用比对照 Tfh 细胞更强(<0.05)。此外,在感染小鼠和可溶性卵抗原(SEA)处理的 Tfh 细胞中均发现 Tfh 细胞凋亡减少(<0.05)。机制研究表明,caspase-3 是感染下调 Tfh 细胞凋亡的主要驱动因素。综上所述,本研究表明,Tfh 细胞的积累可能对疟原虫感染中的免疫反应产生影响,caspase-3 信号介导的凋亡下调可能是导致 Tfh 细胞在该过程中积累的原因。