Lv Y, Wang C, Bai L
Basic Medical College, Dali University, Dali 671000, Yunnan, China.
Key Laboratory of Entomological Biopharmaceutical Research and Development of Yunnan Province, Dali University, Dali 671000, Yunnan, China.
Trop Biomed. 2025 Mar 1;42(1):76-84. doi: 10.47665/tb.42.1.013.
Tuberculosis (TB), an infectious disease caused by the bacterium Mycobacterium tuberculosis (Mtb), is a major cause of morbidity and mortality worldwide. Annually, millions of new cases of tuberculosis are documented. Research in tuberculosis-immune has hitherto focused predominantly on the role of T cells in Mtb infection. Although there have been studies in progress which have supported the notion that B cells are crucial players in combating infectious diseases, the role of B cells in TB is still not fully understood. There is a paucity of in-depth analysis of various B lymphocyte subpopulations and the understanding of the immunophenotypic changes of the B-cell lineage during tuberculosis infection. Therefore, we aimed to investigate the changes in B lymphocyte subpopulations in mice infected with M.tuberculosis H37Ra. The percentage/frequency of peritoneal B cells (CD45R+), B1b cells (CD45RIntIgDCD5- CD11+), splenic B cells (CD45R+), and splenic marginal zone B (MZ B) cells (CD45R+CD23- CD21hi) decreased (P < 0.05), while the percentage of splenic follicular B (Fo B) cells (CD45R+CD23+ CD21int) and lymph node B cells (CD19+) increased at the 4th and 8th weeks (P < 0.05). It was suggested that H37Ra infection changed the distribution of B lymphocyte subpopulations. In addition, the percentage of CD69+B cells and memory B cells (CD45R+CD27+ IgD+/-) increased in the infected mice at different infection periods (P < 0.05), which suggested H37Ra infection promoted B cell activation and produced a large number of memory B cells. As a conclusion, H37Ra infection can affect the distribution of B lymphocyte subpopulations, with a concomitant down-regulation of MZ B cells, which perform innate immunity, and up-regulation of adaptive immune response cells (Fo B cells and lymph node B cells). Furthermore, it has been demonstrated that H37Ra infection can promote the immune response of B lymphocytes to tuberculosis, through the stimulation of the body to produce a large number of activated and memory B cells.
结核病（TB）是由结核分枝杆菌（Mtb）引起的一种传染病，是全球发病和死亡的主要原因。每年都有数百万人被记录为新发结核病病例。迄今为止，结核病免疫研究主要集中在T细胞在Mtb感染中的作用。尽管已有研究支持B细胞在抗击传染病中起关键作用的观点，但B细胞在结核病中的作用仍未完全了解。目前缺乏对各种B淋巴细胞亚群的深入分析，以及对结核病感染期间B细胞谱系免疫表型变化的认识。因此，我们旨在研究感染结核分枝杆菌H37Ra的小鼠中B淋巴细胞亚群的变化。腹腔B细胞（CD45R+）、B1b细胞（CD45RIntIgDCD5-CD11+）、脾B细胞（CD45R+）和脾边缘区B（MZ B）细胞（CD45R+CD23-CD21hi）的百分比/频率降低（P<0.05），而脾滤泡B（Fo B）细胞（CD45R+CD23+CD21int）和淋巴结B细胞（CD19+）的百分比在第4周和第8周增加（P<0.05）。提示H37Ra感染改变了B淋巴细胞亚群的分布。此外，感染小鼠在不同感染时期CD69+B细胞和记忆B细胞（CD45R+CD27+IgD+/-）的百分比增加（P<0.05），这提示H37Ra感染促进了B细胞活化并产生了大量记忆B细胞。结论是，H37Ra感染可影响B淋巴细胞亚群的分布，同时下调执行固有免疫的MZ B细胞，并上调适应性免疫反应细胞（Fo B细胞和淋巴结B细胞）。此外，已证明H37Ra感染可通过刺激机体产生大量活化和记忆B细胞来促进B淋巴细胞对结核病的免疫反应。
