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Biomedical subjects

I Scher

Publications and source records attributed to I Scher.

At least 73 records · Page 4Linked to original sources
PubMed1980

Surface immunoglobulin of rabbit peripheral blood lymphocytes: detection of allotypes by fluorescence and rosetting.

Specific anti-allotype reagents were prepared to detect heavy and light chain allotypes on surface immunoglobulin-positive (sIg+) cells from a3a3b4b4, a2a2b5b5 homozygous and a2a2b4b5 heterozygous rabbits. Total sIg+ peripheral blood lymphocytes (PBL) were detected with fluorescein-labeled goat anti-light chain and sheep anti-rabbit Ig reagents. The total sIg+ cells detected with these reagents and the sum of a and b allotypes individually measured with specific fluorescent anti-allotype reagents (a2 + a3 or b4 + b5) were measured more or ess the same when measured by fluorescence-activated cell sorter (FACS) II flow microfluorometry. The data provided no evidence for single cells expressing both allelic allotypes (allelic inclusion). We found that FACS and resetting techniques were generally equally sensitive. However, we detected a greater proportion of total b4+ plus b5+ cells by rosetting than by fluorescence in some PBL preparations from heterozygous b4b5 rabbits. This was not seen with artificial mixtures of b4b4 and b5b5 cells. The nature of these cells is not yet known. Conceivably, they were not scored as lymphocytes by light-scatter analysis on the FACS and hence were not counted, but were indistinguishable from lymphocytes by microscopy.

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

IgD allotypic determinants. II. Determinants expressed on IgD of mice of the b, e, and o Igh-C haplotypes.

Allotypic determinants expressed on membrane IgD of 27 strains of mice representing each of the major Igh-C haplotypes of inbred mice were examined with reagents specific for the IgD of mice of the b, e, and o Igh-C haplotypes. The distribution of two specificities, IgD.44 (Ig5.2) and IgD.37 (Ig5.3), recognized by two monoclonal anti-delta reagents was determined. In addition, a new specificity, IgD.46, expressed on mice of the o Igh-C type, but not of the b or a types, was detected by a BALB/c anti-AL/N spleen cell antiserum. The results also confirmed the description of the new Igh-C haplotype o, by demonstrating that the mice of this group express the IgD.37 determinant. This determinant is also expressed by mice of the b and e types, but not by mice of the d haplotype, from which the o haplotype was subdivided.

Animals↗
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↗
PubMed1980

Distribution of complement receptors on human normal and malignant mononuclear cells.

Mononuclear cells from normal human subjects and patients with chronic lymphocytic leukemia (CLL), chronic lymphosarcoma cell leukemia (LCL), and hairy cell leukemia (HCL) were labeled with fluoresceinated, purified human C3b (FI-C3b) and analyzed using the fluorescence-activated cell sorter (FACS). FI-C3b labeled 17.6% +/- 6.0% of peripheral blood mononuclear cells (PBM) from 20 normal subjects, which, when separated by the FACS, consisted of B lymphocytes and approximately 5% monocytes. Analyses in which either monocytes or B lymphcoytes were excluded from consideration demonstrated that both these cell types were labeled by the FI-C3b with a heterogeneous distribution of fluorescence intensity, indicating either heterogeneity of CR density or variable avidity of individual CR for the FI-C3b. FACS profiles of PBM ( < 5% monocytes) from 14 of 15 patients with CLL showed a homogeneous distribution of very low fluorescence intensity, with > 60% of the cells being slightly more fluorescent than unlabeled controls. This low, homogeneous distribution of fluorescence is strikingly similar to profiles of CLL cells labeled with anti-Ig reagents and suggests homogeneity of low CR density and/or avidity. Similarly, CR+ mononuclear cells from five patients with HCL and three patients with LCL displayed more homogeneous FI-C3b labeling than normal CR+ PBM. Homogeneity of FI-C3b binding to CLL, LCL, and HCL cells further supports the concept for a clonal origin for these disorders.

Blood Cells↗
PubMed1980

Mapping of the X-linked immune deficiency mutation (xid) of CBA/N mice.

CBA/N mice carry a recessive mutation at the X-linked immune deficiency (xid) locus that precludes their response to certain thymus-independent (TI) antigens. We have determined that xid is situated on the X-chromosome between the genes Ta (tabby) and Hyp (hypophosphatemia), genetic distances being Ta-6.6 +/- 1.8-xid-12.2 +/- 2.3-Hyp.

Animals↗
PubMed1979

Role of a nonimmunoglobulin cell surface determinant in the activation of B lymphocytes by thymus-independent antigens.

Lyb 5 is a B-cell alloantigen which is expressed on 50-60% of B cells. It was defined originally on the basis of cytotoxicity. We have described a new reactivity within the anti-Lyb 5 serum on the basis of selective inhibition of antibody responses in vitro by this antiserum in the absence of complement. This inhibitory activity of anti-Lyb 5.1 serum appears to be due to recognition of antigenic determinants different from the prototype antigens detected in the cytotoxicity assay. Anti-Lyb 5 serum incorporated into spleen cell cultures selectively inhibits antibody responses to a class of thymus-independent antigens (TI-2) previously characterized by their failure to elicit antibody formation in immature mice or in the defective CBA/N strain. Responses to optimal concentrations of TI-1 antigens, which can induce antibody synthesis in these mice, are unaffected by the addition of anti-Lyb 5.1 serum. The B-cell alloantigen defined by this functional assay is designated tentatively Lyb 7 and it is shown to be distinct from cell surface immunoglobulins. Lyb 7 appears to have a role in the activation of B lymphocytes by the TI-2 class of thymus-independent antigens.

Antibody Formation↗
PubMed1979

Endotoxin lethality and tolerance in mice: analysis with the B-lymphocyte-defective CBA/N strain.

Immune-defective and immunologically normal F1 mice derived from the CBA/N strain were used to study the influence of anti-endotoxin antibody on the lethal effects of endotoxin. Immune-defective F1 male mice were unable to make specific responses to purified preparations of E. coli O111:B4 endotoxin, whereas their immunologically normal F1 female littermates made excellent responses. The ability to form antibody to lipopolysaccharide (LPS) in these F1 mice did not influence either their natural resistance to endotoxin challenge or the effects of pretreatment with sublethal amounts of endotoxin on subsequent challenge with higher normally lethal doses. Furthermore, transfer of sera with high titers of anti-LPS antibody to mice prior to challenge with LPS failed to protect. Thus, anti-LPS antibody does not appear to play a critical role in protection of immune-defective (CBA/N X DBA/2) F1 male mice to the lethal effects of endotoxin or to the protective effects of a single sublethal dose of endotoxin on subsequent endotoxin challenge.

Animals↗
PubMed1979

Effect of silica on the innate resistance of inbred mice to Salmonella typhimurium infection.

The role of macrophages in the innate immunity of (CBA/N female X DBA/2N male)F1 female mice to Salmonella typhimurium was assessed with silica, an agent which has been reported to selectively inactivate macrophages. Silica, administered intravenously to mice, markedly decreased the phagocytic capacity of splenic macrophages but had no effect on splenic responsiveness to the B-cell mitogen lipopolysaccharidide or the T-cell mitogen phytohemagglutinin, nor did it affect the frequency of surface immunoglobulin-positive cells (B cells). Silica given to mice 1 day before intraperitoneal challenge decreased the 50% lethal dose of S. typhimurium 100-fold. The incidence of survival of mice given silica up to 14 days before infection with a sublethal dose of organisms was also decreased. This susceptibility could also be demonstrated when silica was given 10 days, but not 20 days, after S. typhimurium infection. Poly-2-vinylpyridine-N-oxide, a lysosomal stabilizing agent, abrogated the silica effect. Deaths among silica-treated mice followed uncontrolled multiplication of the organism in the spleen. These results provide direct evidence that macrophages play an essential role in natural immunity to murine typhoid and demonstrate the efficacy of silica as a tool to analyze macrophage function.

Animals↗