Depletion of peritoneal CD5+ B cells has no effect on the course of Leishmania major infection in susceptible and resistant mice.
The mouse peritoneal cavity contains a unique self-renewing population of B cells (B-1) derived from fetal liver precursors and mainly producing polyreactive antibodies. Since B-1 cells are a potential source of IL-10, it has been suggested that these cells may contribute to the susceptibility of BALB/c mice to Leishmania major infection by skewing the T helper cell network towards a Th2 phenotype. Accordingly, L. major infection of B cell-defective BALB/c Xid mice (lacking B-1 cells) induces less severe disease compared with controls. However, in addition to the lack of B-1 cells, the Xid immune deficiency is characterized by high endogenous interferon-gamma (IFN-gamma) production. In the present study, the role of B-1 cells during L. major infection was investigated in mice experimentally depleted of peritoneal B-1 cells. Six weeks old C57Bl/6 and BALB/c mice were lethally irradiated and reconstituted with autologous bone marrow which allows systemic depletion of B-1 cells. Untreated BALB/c, C57Bl/6 as well as BALB/c Xid mice were used as controls. After reconstitution, mice were injected with L. major amastigotes and progression was followed using clinical, parasitological and immunological criteria. As previously reported, BALB/c Xid mice showed a significant reduction in disease progression. In contrast, despite the dramatic reduction of B-1 cells, B-1-depleted BALB/c mice showed similar or even worse disease progression compared with control BALB/c mice. No differences were found between B-1-depleted or control C57Bl/6 mice. Our data suggest that the B-1 cells do not contribute to the susceptibility of BALB/c mice to L. major infection.
Laboratory of Immunology (LI) (LAF 301), Institut Pasteur de Tunis, Tunis-Belvédère, Tunisia.
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Babai
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Louzir
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Dellagi
D000199:Actins / Q000276:immunology; D000818:Animals; D001323:Autoantibodies / Q000097:blood / Q000276:immunology; D016175:B-Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology; D018956:CD5 Antigens / Q000032:analysis*; D018450:Disease Progression; D005260:Female; D020022:Genetic Predisposition to Disease; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D007153:Immunologic Deficiency Syndromes / Q000235:genetics / Q000276:immunology; D016753:Interleukin-10 / Q000378:metabolism; D018320:Leishmania major / Q000276:immunology* / Q000302:isolation & purification; D016773:Leishmaniasis, Cutaneous / Q000235:genetics / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D018655:Lymphocyte Count; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D010529:Peritoneal Cavity / Q000166:cytology*; D016176:T-Lymphocyte Subsets / Q000276:immunology
D000199:Actins; D001323:Autoantibodies; D018956:CD5 Antigens; D007074:Immunoglobulin G; D016753:Interleukin-10