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B Ardman

Publications and source records attributed to B Ardman.

25 records · Page 2Linked to original sources

Idiotype mimicry by a differentiation antigen on Friend erythroleukemia cells.

We previously found that murine leukemia cells of T cell, B cell, and erythroid ontogeny express a cell membrane antigen that cross-reacts with an idiotype of an anti-retroviral antibody. In the present study, the expression of this antigen (termed AVID, for anti-viral idiotype) by murine erythroleukemia (MEL) cells was examined during chemically induced differentiation. AVID expression by MEL cells was found to be lost when they were treated with either dimethyl sulfoxide or hexamethylene bisacetamide, two chemicals that induce MEL cells to terminally differentiate. The kinetics of disappearance of AVID during inducer treatment reflected the kinetics with which the inducers caused MEL cell commitment to terminal differentiation. Loss of AVID expression by inducer-treated cells was inhibited by dexamethasone, which inhibits commitment and MEL cell differentiation. The subset of inducer-treated cells that expressed the least amount of AVID contained the greatest number of cells committed to differentiate. These results indicate that AVID identifies a novel differentiation antigen of MEL cells.

Acetamides↗

Parallel sets of autoantibodies in MRL-lpr/lpr mice. An anti-DNA, anti-SmRNP, anti-gp70 network.

The public idiotype Id-H130 occurs in MRL-lpr/lpr serum both on a high proportion of anti-DNA autoantibodies as well as on antibodies that do not bind to DNA. To define members of the latter population, we prepared hybridomas and selected Id-H130+ mAbs that did not bind to DNA. One such antibody, mAb 28/12, was found to be an anti-SmRNP antibody. To determine whether mAb 28/12 had rheumatoid factor activity, we tested its ability to bind, in a solid-phase assay, to 16 mouse IgM mAbs. mAb 28/12 bound to only four of the panel, two anti-DNA antibodies (mAbs 512 and 319) and two anti-gp70 antibodies (mAbs 514 and 1417). In a liquid-phase competition assay with a panel of 32 monoclonal IgM and IgG antibodies, including allotype-matched Igs, mAb 28/12 reacted only with mAbs 512, 319, 514, and 1417. The binding of mAb 28/12 to mAbs 512 and 319 was displaced by DNA, but not by RNA, indicating that the idiotype it defines (Id-28/12) is in the antigen-binding region of the two anti-DNA antibodies. In the two anti-gp70 antibodies (mAbs 514 and 1417), Id-28/12 seems to occur in the framework region. To determine if all four Id-28/12+ antibodies shared a common antigen-binding property, they were tested for their ability to react with DNA and gp70. The two anti-gp70 antibodies did not bind to DNA. However, the two anti-DNA antibodies were found to immunoprecipitate viral proteins from retrovirus-infected cells. mAb 512 reacted with gp70, both in cell membrane lysates and in purified form; mAb 319 reacted with gp85, which contains both gp70 and the retroviral protein p15. Antibodies with properties similar to those of mAb 28/12 were found in MRL-lpr/lpr serum. It was possible, by affinity chromatography on an anti-gp70 antibody column, to isolate from serum those anti-(anti-gp70) antibodies with anti-SmRNP activity. These results show that parallel sets of autoantibodies, which share a common idiotype, but which bind to different autoantigens, occur in MRL-lpr/lpr mice. Some populations of anti-DNA, anti-SmRNP, and anti-gp70 antibodies appear to constitute a network of autoantibodies in that strain. We speculate that part of the anti-SmRNP population of autoantibodies can arise by mutation of germline-encoded anti-DNA antibodies.

Animals↗

Dot immunobinding assay for detection of human immunodeficiency virus-associated antigens.

The detection of human immunodeficiency virus (HIV)-associated antigens was simplified by the application of dot immunobinding on a nitrocellulose matrix. Antigens were detected by applying the polyethylene glycol-precipitated supernatants of experimentally infected cultures directly onto nitrocellulose strips and sequentially incubating the strips with an anti-HIV antiserum and an alkaline phosphatase-conjugated, species-specific antiserum. The immune reaction was developed by adding the precipitable substrate indoyl phosphate. The dot immunobinding assay was nearly as sensitive as the reverse transcriptase assay in detecting HIV antigens in experimentally infected peripheral blood mononuclear cells, as well as in a T-cell line. The technique was also useful in the in vitro evaluation of antiviral agents. The dot immunobinding assay is a simple and sensitive technique that is useful in the detection of HIV antigens in studies of viral pathogenesis.

Antigens, Viral↗

Recognition of a leukemia-related antigen by an antiidiotypic antiserum to an anti-gp70 monoclonal antibody.

The possibility that receptors for retroviral gp70 share structural elements with the antigen-binding sites of anti-retroviral gp70 antibodies was investigated. A monoclonal antibody (1416) was produced that reacted with the gp70 of a cloned recombinant leukemogenic retrovirus, termed P1. An antiidiotypic antiserum raised to 1416 was tested for its ability to bind to the thymic leukemia induced by P1 (P1 Thy). A membrane structure was identified on the surface of P1 Thy that reacted with the antibody against the idiotypic determinant of 1416. A similar structure was identified on the surface of several different, independently derived murine leukemias of T cell, B cell, and erythroid lineage. The expression of the idiotype-like determinant on these leukemia cells was independent of the serological relatedness of their expressed retroviral envelope glycoproteins to P1 gp70. The determinant recognized by the antiidiotype was not detected on normal lymphoid cells. The recognition by the anti-(anti-gp70) idiotype of determinants on unrelated murine leukemias suggests that receptors for different leukemogenic viruses may share common structures.

Animals↗

Characterization of thymic lymphoid-stromal cell complex-forming cells in preleukemic AKR mice.

A small population of normal thymic lymphocytes, like the majority of thymic leukemia cells, formed cellular complexes with thymic epithelium-like stromal cells in pseudoemperipolesis. The properties of the complex-forming cells in preleukemic AKR thymus were analyzed after separation of the cells into subpopulations on the basis of cell size and surface antigen expression by using a fluorescence-activated cell sorter. Complex-forming ability was associated with large cells and the following phenotypes: high Thy-1.1, low brain associated theta antigen, high H-2Kk, high Lyt-1, high gp70 and Ia negativity. These properties coincide in general with those of blast cells in the subcapsular zone of the thymus, which have been shown to consist mostly of complex-forming cells. The possible significance of complex formation of normal and leukemic thymocytes with thymic stromal cells is discussed.

Animals↗