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A Trypanosoma cruzi Alkaline Antigen Induces Polyclonal B‐Cell Activation of Normal Murine Spleen Cells by T‐Cell‐Independent, BCR‐Directed Stimulation
Author(s) -
Montes Cl,
Elina I. Zúñiga,
Paola Minóprio,
E Vottero-Cima,
Adriana Gruppi
Publication year - 1999
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1999.00577.x
Subject(s) - cd40 , microbiology and biotechnology , biology , t cell , antigen , antigen presenting cell , b cell , cell growth , antibody , cytotoxic t cell , chemistry , immunology , immune system , in vitro , biochemistry
We have previously reported that a cytosolic alkaline fraction (FI) obtained from epimastigotes of Trypanosoma cruzi promotes the activation, proliferation and differentiation of normal murine B cells into antibody‐secreting plasmocytes. Neither the mechanism nor the cells involved in the FI‐induced polyclonal B‐cell activation were established. In this work we report that accessory cells are required for FI‐induced polyclonal B‐cell activation as no proliferative responses were obtained following treatment of normal spleen mononuclear cells (NSMC) with l ‐leucine methyl ester. Furthermore, FI did not induce the expression of CD25 on T cells and it promoted the proliferation of a T‐cell‐depleted population, indicating that it acts in a T‐independent manner. We observed that NSMC were stimulated in vitro by FI‐released cytokines, such as interleukin (IL)‐4, IL‐6 and IL‐10, which are involved in B‐cell proliferation and differentiation. Interestingly, while significant amounts of interferon‐γ (IFN‐γ) were found in culture supernatants we did not observe detectable levels of IL‐2. Additionally, we found that B‐cell receptor (BCR) and major histocompatibility complex (MHC) class II antigens were involved in the proliferative response induced by FI because antibodies directed against cell‐surface immunoglobulin M (IgM), CD45 and MHC class II molecules inhibited the FI‐induced B‐cell proliferation. CD40 ligand (CD40L) did not participate in such a phenomenon.