Leishmania tropica: Association of a B-cell mitogen with hypergammaglobulinemia in mice |
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Authors: | Jonathan Weintraub Michael Gottlieb Frederic I. Weinbaum |
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Affiliation: | The Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, 20205, U.S.A.;The Laboratory of Microbial Immunity, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20205, U.S.A. |
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Abstract: | Infection of BALB/c mice with Leishmania tropica NIH S strain resulted in splenic enlargement, hypergammaglobulinemia, and polyclonal activation of B lymphocytes as measured by the splenic plaque-forming cell response (PFC) to trinitrophenyl (TNP) and sheep erythrocytes (SRBC). The peak anti-SRBC PFC response occurred 5 weeks after infection; both direct and indirect (facilitated) plaques were significantly increased. The in vitro primary immune response to trinitrophenyl haptenated lipopolysaccharide (TNP-LPS), as enumerated by the anti-TNP PFC response, was also increased on a per-spleen basis beginning 3 weeks after infection. The properties of a lysate of L. tropica promastigotes (LTL) was studied to determine whether polyclonal B-cell activation was related to a parasite-derived mitogen. A B-cell mitogen was identified in LTL which stimulated the proliferation of spleen cells in vitro from uninfected control and congenitally athymic (T-cell-deficient) but not from μ-suppressed (B-cell-deficient) animals. Preliminary characterization of the mitogen material indicated that it was a nonpyrogenic, heat-labile peptide or protein and was probably not bacterial lipopolysaccharide (LPS). |
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Keywords: | Protozoa, parasitic Mouse, inbred strains Mouse, nude Mouse, B-cell deficient Hypergammaglobulinemia Polyclonal B-cell activation Mitogen, B-cell, parasite origin |
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