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Infection and Immunity, February 2002, p. 812-819, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.812-819.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Fas Ligand-Expressing B-1a Lymphocytes Mediate CD4⁺-T-Cell Apoptosis during Schistosomal Infection: Induction by Interleukin 4 (IL-4) and IL-10

Steven K. Lundy^, and Dov L. Boros^*

Department of Immunology and Microbiology, Wayne State University, School of Medicine, Detroit, Michigan 48201

Received 4 September 2001/ Returned for modification 1 November 2001/ Accepted 9 November 2001

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.

Editor: W. A. Petri, Jr.

Present address: Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109

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