ArticleInfection and immunity2002
Fas ligand-expressing B-1a lymphocytes mediate CD4(+)-T-cell apoptosis during schistosomal infection: induction by interleukin 4 (IL-4) and IL-10.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 108 citations in OpenAlex.
- Article
- Conditional Ablation of PKCλ/ι in CD4Biomolecules · 2025Article
- Mechanisms of Interleukin-10-Mediated Immunosuppression in Viral Infections.Pathogens (Basel, Switzerland) · 2025Review
- Frontiers and Controversies in De Novo Gastrointestinal Tumors After Organ Transplantation: Current Progress and Future Directions.Annals of surgical oncology · 2025Review
- Eggs of Schistosoma japonicum deposited in the spleen induce apoptosis of splenic T cells in C57BL/6 mice.Parasitology research · 2025Article
- Review
- Suppressive mechanisms of regulatory B cells in mice and humans.International immunology · 2023Article
- Homeostatic role of B-1 cells in tissue immunity.Frontiers in immunology · 2023Review
- TCDD attenuates EAE through induction of FasL on B cells and inhibition of IgG production.Toxicology · 2021Article
- Regulatory B cells: TIM-1, transplant tolerance, and rejection.Immunological reviews · 2021Review
- Regulatory B Cell Therapy in Kidney Transplantation.Frontiers in pharmacology · 2021Review
- The Dynamics of B Cell Aging in Health and Disease.Frontiers in immunology · 2021Review
- Regulatory B Cells: Role in Type 1 Diabetes.Frontiers in immunology · 2021Review
- Immunosuppressive Mechanisms of Regulatory B Cells.Frontiers in immunology · 2021Review
- Characterization and Activation of Fas Ligand-Producing Mouse B Cells and Their Killer Exosomes.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Immunoglobulin profile and B-cell frequencies are altered with changes in the cellular microenvironment independent of the stimulation conditions.Immunity, inflammation and disease · 2020Article
- B cells induced by Schistosoma japonicum infection display diverse regulatory phenotypes and modulate CD4Parasites & vectors · 2020Article
- Phenotypes, Functions, and Clinical Relevance of Regulatory B Cells in Cancer.Frontiers in immunology · 2020Review
- Antigen-dependent interactions between regulatory B cells and T cells at the T:B border inhibit subsequent T cell interactions with DCs.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020Article
- Differential responses of epithelial cells from urinary and biliary tract to eggs of Schistosoma haematobium and S. mansoni.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
A previous study of the murine model of Schistosoma mansoni infection has implicated splenic CD19(+) B lymphocytes as Fas ligand (FasL)-bearing mediators of CD4(+) T-lymphocyte apoptosis. The present study shows that B-cell deficiency leads to decreased CD4(+) T-cell apoptosis during infection and compares FasL expression and killer function of B-1a- and CD5(-) B-lymphocyte subsets. B-1a cells from uninfected mice displayed constitutive expression of FasL compared with that of CD5(-) B cells. FasL expression was enhanced following worm egg deposition and antigenic stimulation on both subsets of B cells. Purified B-1a cells from uninfected mice were potent effectors of CD4(+) T-cell apoptosis, and the killing effect was enhanced during schistosome infection. FasL expression by splenic B cells required CD4(+)-T-cell help that was replaced by addition of culture supernatants from antigen-stimulated splenocytes of infected mice. The culture-supernatant-stimulated FasL expression was inhibited by anti-interleukin 10 (IL-10) and anti-IL-4 antibodies. Culture of purified B cells with recombinant IL-4 (rIL-4), rIL-10, and soluble egg antigens (SEA) led to increased expression of FasL on B-1a cells. These results suggest that FasL-expressing, splenic B-1a cells are important mediators of SEA-stimulated CD4(+)-T-cell apoptosis and that maximal FasL expression on B-1a cells is dependent on antigenic stimulation and the presence of IL-4 and IL-10.
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