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Biomedical subjects

F Melchers

Publications and source records attributed to F Melchers.

At least 145 records · Page 8Linked to original sources
PubMed1987

Localization of the murine lambda 5 gene on chromosome 16.

The chromosomal location of the murine lambda 5 gene was analyzed by Southern hybridization using restriction enzyme-digested DNA from a panel of 15 mouse X hamster somatic cell hybrids. Sequences homologous with those of lambda 5 DNA were detected in DNA of 5 hybrids. In all 5 hybrids lambda 5 was contained in restriction fragments of equal sizes, the lengths of which indicated that the germline configuration of lambda 5 with three exons and the restriction sites expected from its genomic structure were present. Southern hybridization with the murine lambda 1 gene as a probe detected the same 5 hybrids as positive. The only mouse chromosome present on all of the positive hybrids, and absent from negative ones, was number 16. We conclude that lambda 5 is situated on the same chromosome as lambda 1, i.e., on the murine chromosome 16.

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PubMed1986

Isolation of a cDNA copy of an RNA species expressed in murine pre-B cells.

A part of a gene, pZ 183, was isolated from a cDNA library constructed from poly(A)-containing RNA of the chemically induced murine pre-B lymphoma 70Z/3. This DNA sequence was found to be present in one of 5,000 cDNA clones in the unsubtracted library, and in one of 350 cDNA clones in a library in which sequences common to 70Z/3 and to a T cell hybridoma had been subtracted. This indicates that the corresponding gene belongs to the genes which are expressed with low to medium abundance in the pre-B cell line 70Z/3. The gene was found to be expressed in pre-B lymphomas, but not in B lymphomas, myelomas, T cell lymphomas, macrophage tumors or a fibroblast line. By in situ hybridization it was detected in 2-4% of fetal liver cells between day 15 and 16 of gestation, and in 1% of adult bone marrow cells. It was not detected in thymus cells, nor in mature T cells, spleen, adult liver, kidney, heart, lung or brain. The size of the transcript found in all pre-B cell lymphomas is 1.2 kb in length. The pZ 183 DNA sequence would appear to be a useful B-lineage specific marker which identifies pre-B cells at various stages before the mature B cell.

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PubMed1986

Cell cycle control of activated, synchronized murine B lymphocytes--roles of macrophages and complement C3.

Three restriction points control the cell cycle of activated murine B lymphocytes in a synergistic way. The first is controlled by the occupancy of surface immunoglobulin either by antigen- or by immunoglobulin-specific antibodies. The second is controlled by the complement C3d receptor CR2 which can be occupied by cross-linked C3b or C3d to stimulate the entry into S phase, or by soluble C3d or a C3 alpha-chain peptide, binding to the CR2 receptor, which inhibit the entry into S phase. Macrophages produce so-called alpha factors which also control the B-cell cycle at the same point. Thus, it is suspected that macrophages produce components of the early pathway of complement activation which finally lead to cross-linking of CR2 receptors on B cells. The third restriction point is controlled by unknown receptors that recognize so-called beta factors produced by helper T lymphocytes.

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PubMed1985

The action of human C3 in soluble or cross-linked form with resting and activated murine B lymphocytes.

The third component of complement C3 has been implied in the stimulation of B lymphocytes to proliferation and maturation for Ig secretion. We have reinvestigated the extent of this activation with either activated or resting murine splenic lymphocytes in serum-substituted cultures. Human C3 was used in either soluble or cross-linked form. Soluble as well as Sepharose-bound or glutaraldehyde-cross-linked C3, over a range of concentrations, was inactive with resting splenic lymphocytes of (C57BL/6J X DBA/2)F1, C3H/HeJ and C57BL/6J nu/nu mice. However, lipopolysaccharide-activated spleen cells, enriched for B cell blasts, were stimulated by immobilized and cross-linked C3, while they did not respond to soluble C3. The extent of restimulation was comparable to that induced by lipopolysaccharide and resulted in both increased proliferation and maturation to Ig-secreting cells. The stimulation of the blast cells appears to be C3 specific, since it can be inhibited by free C3.

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PubMed1985

Three restriction points in the cell cycle of activated murine B lymphocytes.

The cell cycle of activated B lymphocytes was found to be controlled by three restriction points. The first occurs immediately after mitosis and was found to be controlled by the binding of Sepharose-bound, immunoglobulin-specific antibodies to surface membrane-bound immunoglobulin. Exposure to this stimulus as short as 15 min or as long as 36 hr allowed B cells to move into the G1 phase up to the next restriction point. The second restriction point was observed to be approximately equal to 4 hr after mitosis, in the G1 phase of the cycle and 3-4 hr before the B cells entered S phase, and was found to be controlled by alpha-type B-cell growth factors produced by the P388D1 macrophage line. A third restriction point occurs in the G2 phase, 2-4 hr before mitosis, and is apparently controlled by beta-type B-cell growth factors that are likely to be produced by helper T lymphocytes.

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PubMed1985

Activation and cell cycle control of murine B lymphocytes.

The cell cycle of activated murine B lymphocytes (B cells) is controlled by the occupancy of surface membrane-bound immunoglobulin (Ig) and by two types of growth factors, called alpha and beta factors. These growth factors are produced in an endocrine fashion by the interaction of helper T lymphocytes (T cells) with antigen-presenting macrophages (A cells). Antigen is taken up, processed and presented on the surface of A cells in the context of class II major histocompatibility complex (MHC) glycoproteins. Helper T cells recognize this association of antigen and class II MHC molecules. A cells produce alpha factors and T cells produce beta factors. The molecular nature of these factors and of the corresponding receptors on B cells has yet to be elucidated, although it can be shown that the complement component C3d replaces alpha factor action. Resting, G0 phase B cells are refractory to the action of alpha and beta factors. They have to be excited, i.e. rendered susceptible to the action of these factors. This can be achieved by the interaction with helper T cells that recognize antigen, bound by surface membrane Ig, in the context of class II MHC glycoproteins on the surface of resting G0 B cells. Excitation can also occur in a polyclonal fashion by cross-linking of surface Ig with immobilized, Ig-specific antibodies, or by the interaction with polyclonal activators of B cells, such as lipopolysaccharides. Entry into the cell cycle is asynchronous. Activated, cycling B cells can be synchronized by size separation, using velocity sedimentation. Synchronized B cells will retain their synchrony for several divisions, when they are stimulated by immobilized Ig-specific antibodies, alpha and beta factors. They divide every 20 h at 37 degrees C. Omission of either of the three stimuli arrests B cells, though at different points in the cell cycle. Three restriction points are found: the first occurs immediately after mitosis and is controlled by the binding of immobilized Ig-specific antibodies to surface membrane-bound Ig.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1984

Monoclonal antibodies specific for murine IgM I. Characterization of antigenic determinants on the four constant domains of the mu heavy chain.

Seventeen monoclonal rat antibodies with specificities for mouse mu heavy chain recognize seven distinguishable determinants that are located on the four constant region domains. All determinants are present on secreted, intracellular and membrane bound IgM, and all but two are expressed on isolated mu heavy chain. One antibody, specific for a site in the first constant region domain, recognizes a determinant that is present on IgM of AKR, C3H/HeJ, C57BL/6J, SJL, DBA/2, BALB/c, NZB and CBA/J mouse strains, but not on IgM of A.TH, A/J and A.CA strains of mice.

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PubMed1984

Pre-B cells in mouse bone marrow: in vitro maturation of peanut agglutinin binding B lymphocyte precursors separated from bone marrow by fluorescence-activated cell sorting.

Peanut agglutinin (PNA) binding by mouse bone marrow cells and fractionation by the fluorescence-activated cell sorter have previously been shown to separate high concentrations of pre-B cells, as identified by cytoplasmic mu-chains (c mu). PNA+ and PNA- marrow cell fractions have now been assayed for the presence of functional pre-B cells able to generate mature B cells in culture, as defined by three criteria, the appearance of cell surface mu-chains (s mu), immunoglobulin secretion in response to bacterial lipopolysaccharides, and B cell colony formation. Small PNA+ cell fractions contained pre-B cells that developed into mature B lymphocytes in 1/2 to 1 day but did not sustain B cell production. Large PNA+ cells included pre-B cells that gave rise to mature B lymphocytes after an interval of 1 1/2 to 3 days and were able to sustain B cell genesis in vitro for at least 3 to 5 days thereafter. PNA- cell fractions contained mature B cells but lacked pre-B cell activity. The results demonstrate that PNA binding allows the separation of functional subsets of pre-B cells from bone marrow and that the three in vitro assays used in this study are closely comparable with one another as functional pre-B cell criteria. The findings suggest correlations between functional assays, c mu expression, PNA receptors, and cell size in characterizing stages of pre-B cell development.

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