The distribution of B lymphocyte subpopulations in mice infected with Mycobacterium tuberculosis H37Ra.

Abstract

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.