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Cross‐linking of surface IgM activates NF‐xB in B lymphocyte
Author(s) -
Rooney John W.,
Dubois Patrice M.,
Sibley Carol Hopkins
Publication year - 1991
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830211214
Subject(s) - protein kinase c , chromosomal translocation , biology , cytoplasm , nf κb , microbiology and biotechnology , antibody , surface immunoglobulin , immunoglobulin m , signal transduction , b cell , lymphocyte , immunology , immunoglobulin g , biochemistry , gene
Abstract In B lymphocytes, cross‐linking of surface IgM activates changes in both the cell cycle and differentiation. In normal B cells and B cell tumors, many stimuli induce the activation of NF‐xB and its translocation from the cytoplasm to the nucleus. In this study we sought to determine if cross‐linking of surface IgM led to the activation of NF‐xB. Our results show that activation of B cells by cross‐linking anti‐IgM antibodies activated NF‐xB in the murine B lymphoid cell lines 70Z/3 and M12, and in the dense fraction of splenic cells. The activation of NF‐xB required optimal doses of anti‐IgM antibodies and took 5 to 10 min to reach maximal levels. Cross‐linking of IgM has also been shown to activate protein kinases including protein kinase C (PKC). To test wether PKC activation was required for NF‐xB translocation, we treated 70Z/3 cells for 18 h with phorbol 12‐myristate 13‐acetate, a procedure which depletes these cells of functional PKC. This treatment did not abrogate the nuclear translocation of NF‐xB following anti‐IgM cross‐linking. These results indicate that the nuclear translocation of NF‐xB is rapidly induced by surface IgM cross‐linking and that this activation appears to use a pathway which does not require PKC.