Faculty Research 1990 - 1999

In the absence of a CD40 signal, B cells are tolerogenic.

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Antibodies, Antibodies-Monoclonal: im, Antigens-CD: im, Antigens-Differentiation-B-Lymphocyte: im, B-Lymphocytes: de, im, CD4-Positive-T-Lymphocytes: im, CD8-Positive-T-Lymphocytes: im, Female, Graft-vs-Host-Reaction: im, Histocompatibility-Antigens-Class-I: im, Histocompatibility-Antigens-Class-II: im, Immune-Tolerance: im, Lipopolysaccharides, Lymphocyte-Culture-Test-Mixed, Membrane-Glycoproteins: im, Mice, Mice-Inbred-Strains, Mice-Knockout, Signal-Transduction: im, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S, T-Lymphocytes-Cytotoxic: im

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Immunity 1995 Jun;2(6):645-53


A126296, CA20408/CA/NCI, CA36860/CA/NCI


When B cells are deprived of signaling through CD40, they exhibit the ability to induce T cell tolerance. The in vivo administration of anti-gp39 and allogeneic B cells diminished the ability of mice to mount an allogeneic response. Tolerance induction was specific for the haplotype expressed on the allogeneic B cells. Selective allospecific unresponsiveness was induced in the CD8 and CD4 compartments by the administration of anti-gp39 and class II-deficient B cells or class I-deficient B cells, respectively. As predicted by studies with anti-gp39 treatment, diminished allospecific responsiveness was induced by the administration of B cells to mice genetically deficient in gp39. Taken together, these data are consistent with the premise that deprivation of CD40 signaling engenders B cells with enhanced tolerogenicity. These studies provide insights into the tolerogenic capacity of resting B cells and outlines a practical approach to exploit this function.

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