Abstract
CD4+ T follicular helper (Tfh) cells, a new subset of immune cells, have been demonstrated to be involved in granulomatous responses to Schistosoma japonicum (S. japonicum) infection. However, the role and underlying mechanisms of Tfh cell aggregation in S. japonicum infection remain incompletely understood. In this study, we provide evidence that S. japonicum 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 (P < 0.05). Furthermore, reduced apoptosis of Tfh cells was found both in S. japonicum infected mice and in soluble egg antigen (SEA) treated Tfh cells (P < 0.05). Mechanistic studies reveal that caspase-3 is the primary drivers of down-regulated apoptotic Tfh cell death in S. japonicum infection. In summary, this study demonstrates that Tfh cell accumulation might have an impact on the generation of immune responses in S. japonicum infection, and caspase-3 signaling mediated apoptosis down-regulation might responsible for the accumulation of Tfh cell in this course.
Highlights
Schistosomiasis remains a devastating public health problem that affects about 240 million people worldwide and more than 700 million persons are at risk of infection, especially in developing countries [1]
Lymphocytes from different immune organs, such as liver, spleen and lymph node, and peripheral blood were isolated from mice in the control and the infected groups and stained as described in Materials and Methods
Results showed that the ratio and absolute number of T follicular helper (Tfh) cells in the organs of the infected mice increased significantly (P < 0.05, Figures 1C–E)
Summary
Schistosomiasis remains a devastating public health problem that affects about 240 million people worldwide and more than 700 million persons are at risk of infection, especially in developing countries [1]. The eggs released by S. japonicum will deposited in the body, such as liver, lung, and enteric wall, which later cause the organ pathologies including granuloma and fibrosis, and lead to organ failure [2]. The deposited worm eggs secreting soluble egg antigen (SEA) could induce a Th2 dominant humoral immune response in both infected human and animals host [3]. Many different types of immune cells, effector molecules, and numerous cytokines are involved in the development or progression of the disease [4,5,6,7]. There is no single marker for distinguishing Tfh cells from other CD4 subsets, they are defined by their expression of surface co-stimulatory molecules
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