Abstract

Toll-like receptors (TLRs) play an important role in regulating immune responses during pathogen infection. However, roles of TLRs on T cells reside in the mesenteric lymph node (MLN) were not be fully elucidated in the course of S. japonicum infection. In this study, T lymphocytes from the mesenteric lymph node (MLN) of S. japonicum-infected mice were isolated and the expression and roles of TLR2, TLR3, TLR4, and TLR7 on both CD4+ and CD8+ T cells were compared. We found that the expression of TLR7 was increased in the MLN cells of S. japonicum-infected mice, particularly in CD4+ and CD8+ T cells (P < 0.05). R848, a TLR7 agonist, could enhance the production of IFN-γ from MLN T cells of infected mice (P < 0.05), especially in CD8+ T cells (P < 0.01). In TLR7 gene knockedout (KO) mice, the S. japonicum infection caused a significant decrease (P < 0.05) of the expression of CD25 and CD69, as well as the production of IFN-γ and IL-4 inducted by PMA plus ionomycin on both CD4+ and CD8+ T cells. Furthermore, the decreased level of IFN-γ and IL-4 in the supernatants of SEA- or SWA-stimulated mesenteric lymphocytes was detected (P < 0.05). Our results indicated that S. japonicum infection could induce the TLR7 expression on T cells in the MLN of C57BL/6 mice, and TLR7 mediates T cell response in the early phase of infection.

Highlights

  • Schistosomiasis is a chronic, parasitic disease caused by blood flukes with significant morbidity and mortality, especially in vertebrates, including humans [1]

  • The bigger size of mesenteric lymph node (MLN), which contained a greater number of CD3+ T cells, was found in the S. japonicum-infected B6 mouse

  • These results suggested that S. japonicum infection could induce strong immune response in intestinal tract

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Summary

Introduction

Schistosomiasis is a chronic, parasitic disease caused by blood flukes with significant morbidity and mortality, especially in vertebrates, including humans [1]. Immunopathological studies have shown that schistosomiasis results predominantly from the evoked host immune response to schistosome eggs and the granulomatous reaction [2]. Schistosomula and its eggs migrate through a variety of tissues, such as the skin, lung [3], liver [4, 5], and intestinal and vesical mucosa [6]. Schistosoma eggs must migrate from the mesenteric vessels, across the intestinal wall and into the feces. A vast proportion of eggs fail to leave their definite host, instead becoming lodged within intestinal or hepatic tissue, where they could evoke potentially lifethreatening pathology [7]. The mesenteric lymph node (MLN) is the main draining lymph node in mouse enterocoelia which contains many types of immune cells [8]. MLN has been associated with initiation of immunological responses to bacterial translocation

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