{"title":"Eggs of Schistosoma japonicum deposited in the spleen induce apoptosis of splenic T cells in C57BL/6 mice.","authors":"Yanjuan Wang, Yuan Hu, Jing Zhang, Danling Zhou, Yanjun Zhang, Jianping Cao","doi":"10.1007/s00436-025-08474-4","DOIUrl":null,"url":null,"abstract":"<p><p>To explore the relationship between Schistosoma japonicum egg deposition and the resultant structural damage to the spleen, mice were infected percutaneously with cercariae or eggs were surgically injected into their spleens. Terminal transferase dUTP nick-end-labeling (TUNEL) showed that cells around the S. japonicum eggs were apoptotic in vivo. Flow cytometry revealed a sharp reduction in splenic B and T cells at 8 weeks post-infection (p.i.) and a significant increase in Annexin V positive T cells. Immunochemistry showed that the remaining follicles in the spleen at 16 weeks p.i. comprised mainly B lymphocytes. Comparing T lymphocytes in the spleen and liver egg granulomas showed obvious CD3<sup>+</sup> positive areas in the spleen, indicating that splenic egg granulomas have a different cellular composition to liver granulomas. S. japonicum eggs deposited in the spleen might induce apoptosis of splenic cells, especially T lymphocytes. When splenic lymphocytes were cultured in vitro with S. japonicum soluble egg antigen (SEA), more cells underwent apoptosis at an antigen concentration of 120 μg/ml compared to 60 μg/ml at all times p.i.. Cells from 8 weeks p.i. seemed more susceptible to SEA-induced apoptosis. Further research should be focus on the molecule(s) that induce T cells apoptosis, which might provide clues to the mechanisms of immunosuppression during S. japonicum infection and will promote vaccine research.</p>","PeriodicalId":19968,"journal":{"name":"Parasitology Research","volume":"124 3","pages":"31"},"PeriodicalIF":1.8000,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11891099/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Parasitology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00436-025-08474-4","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PARASITOLOGY","Score":null,"Total":0}
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Abstract
To explore the relationship between Schistosoma japonicum egg deposition and the resultant structural damage to the spleen, mice were infected percutaneously with cercariae or eggs were surgically injected into their spleens. Terminal transferase dUTP nick-end-labeling (TUNEL) showed that cells around the S. japonicum eggs were apoptotic in vivo. Flow cytometry revealed a sharp reduction in splenic B and T cells at 8 weeks post-infection (p.i.) and a significant increase in Annexin V positive T cells. Immunochemistry showed that the remaining follicles in the spleen at 16 weeks p.i. comprised mainly B lymphocytes. Comparing T lymphocytes in the spleen and liver egg granulomas showed obvious CD3+ positive areas in the spleen, indicating that splenic egg granulomas have a different cellular composition to liver granulomas. S. japonicum eggs deposited in the spleen might induce apoptosis of splenic cells, especially T lymphocytes. When splenic lymphocytes were cultured in vitro with S. japonicum soluble egg antigen (SEA), more cells underwent apoptosis at an antigen concentration of 120 μg/ml compared to 60 μg/ml at all times p.i.. Cells from 8 weeks p.i. seemed more susceptible to SEA-induced apoptosis. Further research should be focus on the molecule(s) that induce T cells apoptosis, which might provide clues to the mechanisms of immunosuppression during S. japonicum infection and will promote vaccine research.
期刊介绍:
The journal Parasitology Research covers the latest developments in parasitology across a variety of disciplines, including biology, medicine and veterinary medicine. Among many topics discussed are chemotherapy and control of parasitic disease, and the relationship of host and parasite.
Other coverage includes: Protozoology, Helminthology, Entomology; Morphology (incl. Pathomorphology, Ultrastructure); Biochemistry, Physiology including Pathophysiology;
Parasite-Host-Relationships including Immunology and Host Specificity; life history, ecology and epidemiology; and Diagnosis, Chemotherapy and Control of Parasitic Diseases.