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The present study shows that B-cell deficiency leads to decreased CD4<jats:sup>+<\/jats:sup>T-cell apoptosis during infection and compares FasL expression and killer function of B-1a- and CD5<jats:sup>\u2212<\/jats:sup>B-lymphocyte subsets. B-1a cells from uninfected mice displayed constitutive expression of FasL compared with that of CD5<jats:sup>\u2212<\/jats:sup>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<jats:sup>+<\/jats:sup>T-cell apoptosis, and the killing effect was enhanced during schistosome infection. FasL expression by splenic B cells required CD4<jats:sup>+<\/jats:sup>-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<jats:sup>+<\/jats:sup>-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.<\/jats:p>","DOI":"10.1128\/iai.70.2.812-819.2002","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T09:55:53Z","timestamp":1027763753000},"page":"812-819","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":98,"title":["Fas Ligand-Expressing B-1a Lymphocytes Mediate CD4<sup>+<\/sup>-T-Cell Apoptosis during Schistosomal Infection: Induction by Interleukin 4 (IL-4) and IL-10"],"prefix":"10.1128","volume":"70","author":[{"given":"Steven K.","family":"Lundy","sequence":"first","affiliation":[{"name":"Department of Immunology and Microbiology, Wayne State University, School of Medicine, Detroit, Michigan 48201"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dov L.","family":"Boros","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbiology, Wayne State University, School of Medicine, Detroit, Michigan 48201"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.2.3.250"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1286-4579(99)80090-2"},{"key":"e_1_3_2_4_2","doi-asserted-by":"crossref","first-page":"1050","DOI":"10.4049\/jimmunol.128.3.1050","volume":"128","year":"1982","unstructured":"Boros, D. 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