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      Induction of NF-AT in normal B lymphocytes by anti-immunoglobulin or CD40 ligand in conjunction with IL-4.

      Immunity
      Animals, Antibodies, Anti-Idiotypic, pharmacology, B-Lymphocytes, drug effects, immunology, Base Sequence, CD40 Ligand, Cell Line, Cross-Linking Reagents, Cyclosporine, DNA, genetics, DNA-Binding Proteins, biosynthesis, Enhancer Elements, Genetic, In Vitro Techniques, Interleukin-2, Interleukin-4, Male, Membrane Glycoproteins, metabolism, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Molecular Sequence Data, NFATC Transcription Factors, Nuclear Proteins, Proto-Oncogene Proteins c-fos, Proto-Oncogene Proteins c-jun, T-Lymphocytes, Transcription Factors, Transfection

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          Abstract

          We show here that ligation of surface immunoglobulin or CD40 receptors in conjunction with interleukin-4 induces the nuclear factor of activated T cells (NF-AT) in normal murine B cells, which is inhibited by cyclosporin (CsA). Lipopolysaccharide, which activates B cells by a Ca(2+)-independent, CsA-resistant pathway, does not induce NF-AT. The NF-AT complex in T cells and B cells appears to be identical, comprising both Fos and Jun proteins and the 120 kDa cytosolic component of NF-AT (NF-ATp). Our transfection experiments using a trimerized NF-AT site linked to the minimal IL-2 promoter driving luciferase activity demonstrate that NF-AT is functional in A20 B-lymphoma cells. These results therefore suggest that the induction of NF-AT forms part of the B cell response to both cross-linking antigens and T cell-generated signals.

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