B-Cell suppression in adult mice injected with anti-delta followed by anti-mu mAb.

Cross-linking of surface IgM or IgD B-cell receptors (BCR) with appropriate anti-Ig antibodies induces IgM(high) or IgD(high) B-cell depletion, respectively. The aim of this paper is to analyze how injections of anti-delta followed by anti-mu monoclonal antibodies (mAb) can deplete and suppress B cells and then induce T-independent type 2 antigen tolerance in adult mice even after treatment is stopped. The experimental protocol consisted of three daily injections of anti-delta mAb followed by repeated injections of anti-mu mAb.

Distinct VH repertoires in primary and secondary B cell lymphocyte subsets in the preimmune repertoire of A/J mice: the CRI-A idiotype is preferentially associated with the HSA(low) B cell subset.

The anti-arsonate immune response of A/J mice is characterized by the occurrence of several recurrent idiotypes with a different temporal pattern of expression. The CRI-A idiotype is typically a memory idiotype since it appears late in the primary and dominates the secondary as well as subsequent immune responses. The CRI-C idiotype is present throughout the responses, including the primary one.

Differential inhibition of B-cell development and xenoreactive natural antibody production by administration of anti-mu or anti-delta monoclonal antibodies in adult rats.

Background: Given the role of xenoreactive natural antibodies (XNA) in the pathogenesis of xenograft rejection, we tested whether the administration of anti-mu or anti-delta monoclonal antibodies (mAbs) in adult rats would suppress the generation of XNA.

Methods: Adult LOU/C (Igkappa-1a) rats were treated with anti-mu or anti-delta mAbs after nonlethal total body irradiation and bone marrow transplantation from congenic LOU/C (Igkappa-1b) rats. The differentiation of donor bone marrow (BM)-driven Igkappa-1b+ B cells and XNA production were analyzed.

Hepatoprotective role of interleukin 10 in galactosamine/lipopolysaccharide mouse liver injury.

Background & Aims: Interleukin (IL)-10 is a potent anti-inflammatory cytokine. Its role in modulating liver injury induced by galactosamine and lipopolysaccharide (Gal/LPS) was investigated.

Methods: The effects of recombinant IL-10 (rIL-10), anti-IL-10 monoclonal antibodies, or gadolinium chloride (GdCl3) pretreatment were studied in mice challenged with Gal/LPS.

Modulation of rat B cell differentiation in vivo by the administration of an anti-mu monoclonal antibody.

We have previously described that the administration of an anti-mu mAb to adult rats results in the total depletion of circulating IgM. In the present study we analyzed the cellular mechanisms involved in the depletion of circulating IgM by the administration of an anti-mu mAb to adult rats. Administration of an anti-mu mAb to adult rats led to the cross-linking and internalization of membrane IgM (mIgM) but not mIgD on the surface of B cells.