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A Muraguchi

Publications and source records attributed to A Muraguchi.

80 records · Page 5Linked to original sources
PubMed1980

In vitro induction of IgM secretion and switching to IgG production in human B leukemic cells with the help of T cells.

In vitro stimulation of the B leukemic cells (B-CLL cells) with normal allogeneic T cells plus PWM induced IgM secretion and a switching from IgM to IgG production. Induction of IgM and IgG production in B-CLL cells with T cells was demonstrated by the presence of the same idiotype in induced Ig as that present in the monoclonal IgM protein in the patient's serum. Both T cells and PWM were required for Ig induction in B-CLL cells, and x-irradiated T cells showed the comparable helper effect. T cells and PWM induced not only Ig secretion but proliferation of B-CLL cells. Cell division was essential for the differentiation of the leukemic cells to Ig-producing cells. PWM-induced, antigen-nonspecific helper factor(s) were also effective in the induction of differentiation of the leukemic cells. Variations existed among T cell donors in the capabilities to induce differentiation of the same leukemic cells, suggesting the requirement of matching of acceptors on B-CLL cells and T effector molecules for the induction of Ig production in B-CLL cells.

Aged↗
PubMed1980

In vitro immune response of human peripheral lymphocytes. V. PHA- and protein A-induced human B colony formation and analysis of the subpopulations of B cells.

Human B colony formation was observed with PHA or protein A as a mitogen. Preculture of B cells with mitogens in the presence of irradiated T cells for 3 days was a prerequisite for the induction of B cell colonies. About 300 to 700 colonies per 10(6) seeded cells were detected and a linear relationship between the number of cells seeded and the number of colonies developed was observed. Cells in PHA-induced colonies had surface IgM and/or IgD but no cytoplasmic Ig, whereas cells recovered from protein A-induced colonies had cytoplasmic Igs that were not only IgM but IgG and IgA. In each of the protein A-induced colonies, a sequential appearance of IgM-, IgG-, and IgA-producing cells was observed from day 3 to day 5, showing that IgM-, IgG-, and IgA-producing cells were derived from a single precursor cell. PHA and protein A had an additive effect on the number of colonies induced. About 50% of colonies induced in the presence of both PHA and protein A had Ig-producing cells. These results suggest that PHA and protein A may stimulate distinct subsets of B cells into colony formation.

Animals↗
PubMed1980

In vitro immune response of human peripheral lymphocytes. VI. Distribution and characterization of precursors for PHA- and protein A-induced colony-forming B cells.

B cells from peripheral blood or cord blood formed colonies by stimulation with either PHA or protein A. On the other hand, tonsillar B cells did not form protein A-induced colonies, although PHA-induced colony formation was comparable to that observed in peripheral B cells. Lack of protein A-induced colony formation in tonsillar B cells was not due to the defect of helper T cells in preculture or to the presence of suppressor cells but was due to the absence of precursors for colony formation. The result showed that PHA- and protein A-induced colony-forming cells belonged to distinct subsets of B cells. Depletion of mu-bearing cells from peripheral B cells abrogated both PHA- and protein A-induced colony formation. Depletion of delta-bearing cells did not affect PHA- and protein A-induced colony formation and the population enriched with delta-bearing cells also showed colony formation. Depletion of complement receptor (CR)-positive cells removed precursors for both PHA- and protein A-induced colony formation. These results showed that precursor cells for PHA- and protein A-induced colony formation were IgM+, IgD+ and CR+ or IgM+, IgD- and CR+.

Animals↗
PubMedDate not supplied

A murine monoclonal antibody (928) recognizing a new epitope formed with a combination of HLA-DPA1*0201 and DPB1*0301 gene products.

A murine monoclonal antibody (mAb), 928, that recognizes a cell surface antigen (928 Ag) on a human Epstein-Barr virus-transformed fetal liver-derived lymphoid progenitor cell line (FL4.4) was generated. The 928 mAb reacted with only FL4.4; it did not react with any other 57 cell lines tested. Two color flowcytometry analysis of peripheral blood mononuclear cells (PBMC) revealed that the 928 mAb reacted with B cell and monocyte fractions from only two individuals out of 63 unrelated donors. Biochemical analyses showed that the 928 Ag composes of two molecules (33 and 34 Kd) and forms a SDS-resistant, noncovalently linked dimer conformation, the feature being similar to that of peptide-bound MHC class II molecules. Treatment of FL4.4 cells with the 928 mAb significantly facilitated homotypic cell aggregation. In addition, treatment of PBMC of the 928 Ag+ donor with recombinant IL-4 augmented the expression of the 928 Ag on CD64+ monocytes. Typing of HLA-DRB1, DPA1 and DPB1 alleles of the 928 Ag expressing and nonexpressing cells revealed that the 928 Ag is expressed only on PBMC of HLA-DPA1*0201 and DPB1*0301 positive donors. Finally, anti-DP antibody precleared 928 Ag from the cell lysate. These results demonstrate that the 928 mAb recognizes a polymorphic determinant of HLA-DPA1*0201-DPB1*0301 gene products. The possibility that amino acids in the groove of the peptide-binding site of HLA-DP molecules are critical for the 928 epitope is discussed.

Animals↗
PubMedDate not supplied

Activation and immunoregulation of human B lymphocytes.

Immunocompetent cells communicate via direct cellular contact and/or by the release and binding of soluble mediators. These soluble mediators transmit signals for growth and differentiation of various cell types. We have been intensively studying the regulation of human B lymphocytes and have focused on the events which occur following stimulation of mature, resting B cells with antigen or an antigen equivalent, anti-immunoglobulin antibody. Anti-Ig stimulates resting B lymphocytes to enlarge, synthesize RNA, increase membrane Ia expression, express activation markers, and become responsive to soluble factors termed B-cell growth factors (BCGF). We have described two different BCGFs, an 18 kd BCGF derived from a T-T hybridoma and a 60 kd BCGF derived from a T cell line. Activated B cells in the presence of BCGF further enlarge; express another activation marker, the transferrin receptor; and enter the S phase of the cell cycle, but do not differentiate unless another factor is present, e.g., B-cell differentiation factor (BCDF). We have described another T-T hybridoma which constitutively secretes both an 18 kd BCGF and a 35 kd BCDF. These two factors can easily be separated by biochemical means. The 35 kd BCDF induces the differentiation of activated but not resting B cells. Besides these B-cell-specific factors, we have studied the immunoregulatory effects of interleukin 1 (IL-1), IL-2, and interferons (alpha and gamma) on human B-cell responses. Interleukin 1 weakly co-stimulates resting B cells when it is present with anti-Ig and enhances the differentiation of activated and proliferating B cells when it is present in culture with BCDF. Interleukin 2 receptors as defined by the monoclonal antibody anti-Tac and radiolabeled IL-2-binding assays are present on in vitro activated B cells. Recombinant IL-2 added to cultures of in vitro activated B cells promotes both B-cell growth and B-cell differentiation into Ig-secreting cells. Finally, interferons appear to have little direct effect on human B-cell function. Major advances in our understanding of the complexities of B-cell activation, proliferation, and differentiation have been realized over the past few years. The eventual isolation and chemical characterization of the soluble mediators of B-cell function and the receptors for these mediators should lead to further insights and to new approaches to those diseases characterized by aberrations of B-cell function.

Antigens, Differentiation, B-Lymphocyte↗