TLR7 modulating B-cell immune responses in the spleen of C57BL/6 mice infected with Schistosoma japonicum

PLoS Negl Trop Dis. 2021 Nov 17;15(11):e0009943. doi: 10.1371/journal.pntd.0009943. eCollection 2021 Nov.

Abstract

B cells played an important role in Schistosoma infection-induced diseases. TLR7 is an intracellular member of the innate immune receptor. The role of TLR7 on B cells mediated immune response is still unclear. Here, C57BL/6 mice were percutaneously infected by S. japonicum for 5-6 weeks. The percentages and numbers of B cells increased in the infected mice (p < 0.05), and many activation and function associated molecules were also changed on B cells. More splenic cells of the infected mice expressed TLR7, and B cells were served as the main cell population. Moreover, a lower level of soluble egg antigen (SEA) specific antibody and less activation associated molecules were found on the surface of splenic B cells from S. japonicum infected TLR7 gene knockout (TLR7 KO) mice compared to infected wild type (WT) mice (p < 0.05). Additionally, SEA showed a little higher ability in inducing the activation of B cells from naive WT mice than TLR7 KO mice (p < 0.05). Finally, the effects of TLR7 on B cells are dependent on the activation of NF-κB p65. Altogether, TLR7 was found modulating the splenic B cell responses in S. japonicum infected C57BL/6 mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • B-Lymphocytes / immunology*
  • Female
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Schistosoma japonicum / genetics
  • Schistosoma japonicum / physiology*
  • Schistosomiasis japonica / genetics
  • Schistosomiasis japonica / immunology*
  • Schistosomiasis japonica / parasitology
  • Spleen / immunology*
  • Spleen / parasitology
  • Toll-Like Receptor 7 / genetics
  • Toll-Like Receptor 7 / immunology*

Substances

  • Toll-Like Receptor 7

Grants and funding

This research was supported by grants from the Natural Science Foundation of China (81771696 to JH, 81802024 to HW, 31800739 to QY), the Guangdong provincial education department (2016KZDXM033 to JH), the Natural Science Foundation of Guangdong province (2020A1515010251 to JH, 2018A030313217 to HW), and Guangzhou science and technology plan project (202002030082 to JH, 202102020912 to HW, 202102080014 to QY), the Open Foundation Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education (2021kfkt03), and Medical Research Fund of Guangdong province (A2018492). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.