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F D Finkelman

Publications and source records attributed to F D Finkelman.

At least 235 records · Page 13Linked to original sources
PubMed1982

Interactions between lymphocyte membrane molecules. II. Characterization of an interaction between B lymphocyte surface IgD and Fc IgG receptors that differs from the surface IgM-Fc IgG receptor interaction.

The B lymphocyte surface membrane receptors IgD (sigD) and Fc IgG receptors (Fc gamma R) were evaluated for interactions by means of immunofluorescence. Ligand-(F(ab')2 anti-delta) induced capping of sIgD resulted in co-capping of Fc gamma R if the latter were occupied during the capping process by soluble antigen-antibody complexes (which themselves provided insufficient cross-linking to result in capping), but not if the Fc gamma R were occupied by monomeric IgG or unoccupied. Capping of Fc gamma R by highly cross-linked complexes did not cause co-capping of sIgD occupied by monomeric F(ab') anti-delta. The interaction between sIgD and Fc gamma R was specific in that cross-reactions between ligands were excluded and ligand-induced capping of sIgD did not cause co-capping of ligand-occupied sIgM or I-A antigens. The sIgD-Fc gamma R interaction occurred on only approximately 60% of B lymphocytes, and this B cell subpopulation did not correlate with other B cell subpopulations (CBA/N strain B cells and B cells bearing either large or small amounts of sIgD). The sIgD-Fc gamma R interaction differed from the sIgM-Fc gamma R interaction in that co-redistribution of the Fc gamma R was occupied by monomeric IgG and involved nearly all B lymphocytes. The qualitative and quantitative differences between the sIgD-Fc gamma R and sIgM-Fc gamma R interactions suggest a mechanism whereby the two antigen receptors could provide different signals to the B lymphocyte.

Animals↗
PubMed1982

Neonatal suppression with anti-Ia antibody. I. Suppression of murine B lymphocyte development.

To investigate the role of sIa in B lymphocyte development, mice were injected from birth with hybridoma anti-Ia antibody. There was on the average a 95% reduction in the number of sIgD+ cells, and 85% diminution in the number of sIgM+ cells, a small but significant increase in the number of sIgM+ sIgD- sla- B cells, as well as a dramatic increase in the number of sIgM- cells bearing a B lineage antigen. Exposure of cells to high doses of anti-Ia antibody in vitro or in vivo for 24 hr did not affect the number of sIg+ lymphocytes. Thus, it appears that chronic anti-Ia administration critically alters normal B lymphocyte development.

Animals↗
PubMed1981

IgD-secreting murine plasmacytomas: identification and partial characterization of two IgD myeloma proteins.

We have used an immunofluorescence inhibition assay to identify 2 BALB/c plasmacytomas, TEPC-1017 and TEPC-1033, that secrete large quantitites of IgD. Both TEPC-1017 and TEPC-1033 myeloma proteins bound to anti-kappa as well as hybridoma and heterologous anti-delta antibodies, but not to anti-mu, gamma, alpha, or lambda antibodies. Both myeloma proteins were purified by (NH4)2SO4 precipitation, ion exchange chromatography, gel filtration, and Staphylococcus aureus Protein A absorption. These IgD kappa myeloma proteins were used to prepare affinity purified rabbit antibodies to delta-chain and the TEPC-1017 and TEPC-1033 idiotypes. Native TEPC-1017 and TEPC-1033 both had mobilities between those of mouse IgA kappa dimers and trimers when analyzed by polyacrylamide gradient gel electrophoresis. Both IgD myeloma proteins broke down under mild reducing conditions into subunits with electrophoretic mobilities slightly slower than those of an IgA kappa monomer. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of reduced TEPC-1017 and TEPC-1033 demonstrated kappa-chains and heavy chains that co-migrated with alpha chain. These data suggested that secreted IgD contains 2 delta 2 kappa 2 subunits that are linked by an easily reducible disulfide bond. The kappa-chains of IgD secreted by TEPC-1017 and TEPC-1033 have apparent m.w. of approximately 63,000 daltons, whereas the apparent m.w. of intracytoplasmic delta-chain, intracytoplasmic delta-chain synthesized in the presence of tunicamycin, and the cellfree translation product of TEPC-1017 delta-chain mRNA are 54,000, 43,000, and 44,000 daltons, respectively. This is compatible with the interpretation that the delta-chain peptide has a leader sequence and is N-glycosylated during or shortly after peptide synthesis and is glycosylated further shortly before IgD secretion.

Animals↗
PubMed1981

Increased expression of I-region-associated antigen (Ia) on B cells after cross-linking of surface immunoglobulin.

Both surface Ig (sIg) surface Ia (sIa) have been shown to have important roles in B lymphocyte activation. In order to investigate a possible relationship between these molecules, we studied the effects of cross-linking of sIg on the expression of sIa, as measured by fluorescence-activated cell sorter analysis of lymphoid cells stained with conventional anti-Ia anti-serum or with fluorescein-labeled anti-Ia antibodies. Exposure of cells for 24 hr in vitro to anti-delta, anti-mu, anti-kappa antibodies, or their F(ab')2 fragments induced a very dramatic increase in expression of sIa. Similarly, i.v. injection of anti-delta antibodies into adult mice induced a 2- to 3-fold increase in expression of B cell sIa on spleen, lymph node, and Peyer's patch lymphocytes. There was no increase under these conditions in expression of other B lymphocyte surface antigens, including H-2, 4B9, and 17C9. Furthermore, exposure of B lymphocytes to antibodies directed to B lymphocyte surface antigens other than sIg did not result in an increase in expression of sIa. The anti-Ig-induced increase in sIa expression appeared to be T independent, required cellular protein synthesis, and required more time to occur than did the cross-linking and removal of sIg. This increase in expression of sIa did not occur on B lymphocytes obtained from mice younger than 3 wk old. This increase in expression of sIa may reflect a proximal event in B lymphocyte activation that occurs after cross-linking of sIg by antigen and that may enhance subsequent cellular interactions involving B lymphocytes.

Animals↗
PubMed1980

Mouse immunoglobulin D: construction and characterization of a cloned delta chain cDNA.

TEPC 1017 is a BALB/c plasmacytoma that synthesizes IgD in large enough amounts to permit the isolation of mRNA for mouse delta chains. cDNA has been prepared from this mRNA, and an 880-base-pair fragment of it has been cloned by recombinant DNA techniques. The hybridization selection technique has been used to show that this cDNA clone specifically binds only mRNA that can be translated into immunoprecipitable delta chains. the sequence of a portion of this clone has been determined and, when translated, shows homology with the C delta 3 of a human myeloma protein. Using this cDNA clone as a probe, we have found that several different-sized delta RNAs are present in TEPC 1017 and in another IgD-secreting plasmacytoma, TEPC 1033.

Animals↗
PubMed1980

IgD allotypic determinants. I. Determinants expressed on murine IgD of the a allotype.

Allotypes of membrane IgD of 27 strains of mice were determined with a series of anti-delta reagents, each capable of binding to the IgD of BALB/c spleen cells. One of these reagents is a newly defined allospecific rabbit anti-mouse-delta a. Typing with these reagents reveals the strain distribution of the previously described IgD.36 (Ig5.1) and IgD.43 (Ig5.4) specificities and demonstrates the existence of a new specificity, IgD.45 (Ig5.5). The results confirm the previous subdivision of the Igh-Ce haplotype into Igh-Ce, to which A mice are assigned, and Igh-Cn, to which NZB and NZW mice are assigned. In addition, it is shown that the Igh-Cd haplotype must also be subdivided. AKR mice, which express the a allele at the Igh-5(delta) locus, are designated as possessing the Igh-Cd haplotype while AL/N and C.AL20 mice, which have the e allele at the Igh-5(delta) locus, are assigned a new Igh-C haplotype designation, o.

Absorption↗
PubMed1980

Development of B lymphocytes in the mouse; studies of the frequency and distribution of surface IgM and IgD in normal and immune-defective CBA/N F1 mice.

Affinity-purified anti-mouse mu and delta antibodies and flow microfluorometric techniques were utilized to study the frequency and distribution of sIgM and sIgD on adult and neonatal B lymphocytes of immunologically normal mice and mice with the immune-defect characteristic of the CBA/N strain. Neonatal normal B lymphocytes can be distinguished from their adult counterparts by the presence of increased amounts of sIgM on sIgM+ cells and by the increased number of sIgM+IgD- cells. The most primitive B lymphocytes of immunologically normal mice appear to reside in the bone marrow of 1- to 2-wk-old mice and are distinguished from splenic B lymphocytes at this time by their relatively low amounts of sIgM. However, in the adult, splenic and bone marrow B lymphocytes are indistinguishable with regard to the quantities of their sIgM or sIgD. Adult immune-defective mice have increased amounts of sIgM on their B lymphocytes, although the number of sIgM+ IgD- cells in these mice is not increased. During development, however, larger than normal numbers of sIgM+ IgD- cells are found in the spleen and bone marrow of these mice; and the low frequency of such cells seen in normal adults is not achieved in immune defectives until after the 56th day of life. Thereafter, immune-defective mice have low frequencies of B lymphocytes with high relative amounts of sIgM, even after 1 yr or age.

Animals↗
PubMed1979

Circulating and pokeweed mitogen-induced immunoglobulin-secreting cells in systemic lupus erythematosus.

Peripheral blood mononuclear cells (PBM) obtained from patients with active untreated systemic lupus erythematosus (SLE) were evaluated both for the number of cells spontaneously secreting immunoglobulin (Ig) as well as for their capacity to generate immunoglobulin-secreting cells (ISC) in vitro in response to pokeweed mitogen (PWM). ISC were enumerated by a reverse haemolytic plaque assay designed to quantify the number of cells secreting IgG, IgM and IgA. PBM obtained from eight patients with active untreated SLE contained markedly increased numbers of ISC compared to age-, sex-, and race-matched normal control PBM. SLE PBM contained a mean of 13,805 +/- 3266 ISC per 10(6) cells, of which 74% secreted IgG, 10% IgM and 22% IgA, while normal PBM contained a mean of 779 +/- 143 ISC per 10(6) cells, with 57% secreting IgG, 25% IgM and 33% IgA. PBM obtained from SLE patients were also examined for their ability to generate ISC in vitro in response to PWM. SLE PBM were markedly deficient in their capacity to respond to PWM with the differentiation of ISC. This diminished responsiveness could not be ascribed to serum factors, the presence of increased numbers of cells with suppressive capacity or the absence of potentially responsive B cells. Rather, a deficiency of helper T cell activity appeared to be responsible. This was indicated by the observation that PWM responsiveness could be restored to SLE PBM by co-culturing them with purified mitomycin C-treated normal T cells.

Adolescent↗
PubMed1979

Defective resistance to Plasmodium yoelii in CBA/N mice.

The role of B lymphocytes in resistance to malaria was studied in defective and normal F1 mice derived from CBA/N mice, a strain with an X-linked B cell defect. When infected with normally nonlethal Plasmodium yoelii, immune defective F1 male mice had higher parasitemias and more prolonged infections than normal F1 mice, as well as a 50% mortality rate. Before infection the plasma levels of IgM and IgG were lower in defective F1 males than normal F1 mice. The polyclonal IgM and IgG responses of infected abnormal F1 mice were delayed and lower in absolute magnitude than those of normal F1 mice. Furthermore, specific IgM and IgG anti-plasmodial antibody titers, as determined by radioimmunoassay, were depressed on day 12 in the defective F1 males. Although IgG titers approached those of the normal F1 mice on day 19, defective F1 male IgM titers remained depressed. These data demonstrate that an X-linked gene that affects B cell function influences malarial resistance in mice, presumably via a decreased specific IgM response, and the slow development of a specific IgG response to P. yoelii infection.

Animals↗
PubMed1979

Preparation of an antibody to mouse serum IgD.

Mice have recently been shown to have serum IgD. We have used affinity chromatography to partially purify mouse serum IgD, and have prepared a rabbit antiserum against this mouse Ig class. This antiserum, once adsorbed by IgD-depleted mouse serum bound to Sepharose, was isotype specific as determined by radioimmunoassay and fluorescence activated cell sorter analysis, and bound to the same splenic lymphocyte surface molecules as a hybridoma produced monoclonal anti-mouse delta antibody.

Animals↗