PubMed Health⌕ Search

Biomedical subjects

R Wistar

Publications and source records attributed to R Wistar.

At least 37 records · Page 2Linked to original sources
PubMed1980

Activation of human platelets by antibodies to thymocytes and beta 2-microglobulin. I. Qualitative and quantitative aspects of the platelet aggregation induced by HATG and SA beta 2mG.

The platelet effect of antibody preparations known to have immunosuppressive action was investigated by a turbidimetric method in vitro. Both horse anti-human thymocyte globulin (HATG) and sheep anti-human beta 2-microglobulin IgG (SA beta 2mG) caused the platelets to aggregate in all human platelet-rich plasmas (PRP) tested. The aggregation was usually irreversible and characterized by a sigmoid curve. The action is specific for the antibodies in HATG and SA beta 2mG because control preparations (horse normal IgG and IgG fractions of sheep normal, anti-dog IgG and anti-human IgA sera) were ineffective; further, heating (30 min at 56 degrees C) and BaSO4 or Al(OH)3 adsorption of HATG and SA beta 2mG did not alter their aggregating capability. When HATG and SA beta 2mG were added together to PRP, they induced aggregation in a simple additive manner. High antibody doses tended to decrease the extent of aggregation. The effect of platelet count on aggregation varied with both the dose level ('low' or 'high') and type (HATG or SA beta 2mG) of the inducer antibody. Using fixed submaximal doses, four main aggregation patterns could be recognized among 60 PRP: (i) high responses to both HATG and SA beta 2mG; (ii) high to HATG, low to SA beta 2mG; (iii) low to HATG, high to SA beta 2mG; and (iv) low to both. The results provide guidelines for quantitative aggregation studies with platelet antibodies and suggest that HATG and SA beta 2mG act through distinct platelet membrane components, the receptor for the latter being the best characterized protein of the mammalian cell membrane.

Antibodies↗
PubMed1979

The identification of the subclasses of human IgG by analytical isotachophoresis.

A new method is described for demonstrating the individual subclasses of human IgG immunoglobulins by means of analytical isotachophoresis. Individual subclasses of IgG purified from sera of multiple myeloma patients have distinct mobility patterns. When a mixture with purified IgG for each of the 4 subclasses is analyzed, a characteristic mobility pattern with 4 unique peaks is obtained. An IgG of unknown subclass can be identified by the superimposition of the peak for the unknown upon one of the 4 well characterized peaks. The method using microgram quantities protein in a 1.0 microliter volume can be performed easily in 15 min.

Hemagglutination Tests↗
PubMed1979

Immunological and structural properties of human monoclonal IgG cryoglobulins.

Structural and immunological properties were determined for sixteen IgG and one Bence-Jones, human monoclonal cryoglobulins. The heavy chain subclass percentages were 47% IgG1, 14% IgG2 and 29% IgG3, and were different from previously reported distributions of myeloma proteins. In addition, 69% (eleven out of fifteen) of the cryoglobulins and 100% (seven out of seven) of the IgG1 cryos contained type lambda light chains. Electrofocussing of the cryoproteins by analytical liquid gradient column showed the isoelectric points to be included in the range of pH 6.3--8.9. The pI of six light chains and five out of six heavy chains were at acidic and slightly basic pH, respectively. The pI of the intact cryoglobulins were thus close to those of their constituent heavy chains. Six out of seven of the heavy chains were subjected to automated Edman degradation and were classified as containing vH-i or vH-ii variable region subgroups on the basis of their blocked amino termini. One type lambda light chain was unusual in that it contained an amino terminal sequence initially described in an amyloid fibril protein and is the first instance in which light chains with this sequence have been isolated from IgG. The data support the notion that the cryoglobulins are IgGs with unique structural and immunological properties which separate them from non-cryoprecipitable IgGs.

Amino Acid Sequence↗
PubMed1979

Surface immunoglobulin density on human peripheral blood mononuclear cells.

The densities of surface immunoglobulin (slg) on peripheral blood mononuclear cells (PBM) of normals and patients with chronic lymphocytic leukemia (CLL), chronic lymphosarcoma cell leukemia (LCL), and hairy cell leukemia (HCL) were analyzed using the fluorescence-activated cell sorter (FACS). PBM were labeled with fluorescein conjugates of F(ab')2 fragments of affinity chromatography-purified anti-Fab or class-specific anti-mu, anti-delta, anti-gamma, or anti-alpha. Histograms of relative cell fluorescence, rems of relative cell fluorescence, reflecting slg density, were prepared with the FACS. Anti-Fab-labeled normal PBM demonstrated a homogeneous low-density peak that when separated by the FACS and analyzed cytochemically consisted predominantly of monocytes, whereas brighter-staining cells were predominantly lymphocytes. Anti-mu and anti-delta labeled 9.0% and 8.5% of normal PBM, respectively, the slg+ cells being virtually all lymphocytes. Cells labeled by anti-gamma exhibited low homogeneous slg density and consisted of more than 80% monocytes. No normal or leukemic PBM were labeled by anti-alpha. All slg-positive cells (less than 5% monocytes) from 12 of 13 patients with CLL had very low homogeneous densities of slg and bore slgM, Whereas cells from 9 of 13 and 2 of 13 patients bore slgD and slgG, respectively. Similarly, PBM from 2 patients with HCL exhibited low and homogeneous densities of algM, slgD, and slgG, whereas those from a third patient bore only slgG. By contrast, the density of slgM and PBM derived from 3 patients with LCL was very high; slgD and slgG densities varied from very high to undetectable in these patients. The different homogeneous densities of slg on peripheral blood lymphocytes from patients with CLL, HCL, and LCL suggest that these diseases represent malignant transformation of different B-lymphocyte subpopulations.

Fluorescent Antibody Technique↗
PubMed1977

A Waldenström macroglobulin that is both a cold agglutinin and a cryoglobulin because it binds N-acetylneuraminosyl residues.

A purified human monoclonal IgM(kappa) (cold agglutinin MKV) has been characterized as both a cold agglutinin and a cryoglobulin. Since its reactivity with human erythrocytes but not with dog erythrocytes is reduced by treatment of the cells with ficin and its reactivity with both is abolished by treatment of the cells with neuraminidase, it has by definition Pr(2) specificity [Roelcke, D. (1974) Clin. Immunol. Immunopath. 2, 266-280]. Presumably, the membrane receptors for cold agglutinin MKV are sialic acid-containing glycoproteins in human cells and sialic acid-containing glycolipids in dog cells. Agglutination of erythrocytes is specifically inhibited by II(3)-N-acetylneuraminosyllactosylceramide (GM(3)) and N-acetylneuraminosylparagloboside but not by their N-glycolylneuraminosyl forms or by lactosylceramide or paragloboside, and the reactivity of neuraminidase-treated cells can be restored by allowing them to absorb either GM(3) or N-acetylneuraminosylparagloboside. When large amounts of ganglioside are absorbed, the cells are agglutinated not only in the cold, but also at 37 degrees , showing that the density of receptor sites on the erythrocyte surface can influence the thermal amplitude of cold agglutinins. Liberation of sialic acid from cold agglutinin MKV by treatment with neuraminidase (acylneuraminosyl hydrolase; EC 3.2.1.18) does not affect its agglutinating properties but the asialoprotein is no longer a cryoglobulin. Apparently the physical basis for its precipitation in the cold is the intermolecular immune binding of N-acetylneuraminosyl residues.

Adult↗
PubMed1977

Loss of antibody activity in human immunoglobulin A exposed extracellular immunoglobulin A proteases of Neisseria gonorrhoeae and Streptococcus sanguis.

Immunoglobulin A (IgA) proteases are extracellular enzymes elaborated by Neisseria gonorrhoeae, N. meningitidis, and Streptococcus sanguis. These enzymes each cleave human IgA1 at a critically situated prolyl-threonyl peptide bond to yield Fab alpha and Fc alpha fragments. To study their effect on the antibody activity of human IgA, we enzymatically digested a group of five human IgA monoclonal immunoglobulins with high-titer rheumatoid factor or cold agglutinin activity and human serum macroamylase, an amylase-IgA complex. In contrast to four control IgM rheumatoid factor monoclonal proteins, whose activity was unaffected by enzyme, gonococcal and streptococcal IgA proteases caused prompt, major reductions of IgA antibody activity to negligible levels and converted macroamylase activity to amylase of normal size, as determined by molecular sieve chromatography. In addition, both enzymes promptly deagglutinated sensitized cells that had been aggregated by IgA rheumatoid factors, indicating that IgA bound to antigen is also susceptible to enzyme cleavage. Fab fragments of Iga protein Chr, a rheumatoid factor, showed essentially no antigen-binding activity despite the high titers observed with the parent protein. These studies emphasize the high degree of specificity of the microbial proteases for IgA and their potential for interfering with antibody activity in the IgA1 subclass.

Agglutination↗
PubMed1976

B-lymphocyte heterogeneity: ontogenetic development and organ distribution of B-lymphocyte populations defined by their density of surface immunoglobulin.

The density of total Ig and of IgM, IgG1, IgG2, and IgA on the surface of adult murine splenic B lymphocytes was measured using the technique of rapid flow microfluorometry. In addition, the density of total surface Ig and of IgM on B lymphocytes derived from adult bone marrow, lymph nodes, and Peyer's patches, and from neonatal spleen was determined. Adult spleen and lymph node B lymphocytes are characterized by the presence of a large population of cells with a low-to-intermediate density of total surface Ig, which is seen as a peak in the fluorescence profiles when these cells are labeled with fluorescein-conjugated (F1) anti-Ig. This peak is not detected when neonatal spleen or adult bone marrow are examined; the development of this peak among spleen cells occurs during the first 4 wk of life. Although the characteristic fluorescence intensity peak is not seen when adult spleen cells are labeled with Fl anti-mu, changes in the density of surface IgM do occur during the first few weeks of life and are detected as a decrease in the frequency of cells which have relatively large amounts of surface IgM. The differences seen in the fluorescence patterns of adult spleen cells labeled with Fl anti-Ig and Fl anti-mu may be due to the appearance of IgD on the surface of mature splenic B lymphocytes. This is supported by the similarity of the fluorescence profiles of adult bone marrow cells stained with Fl anti-Ig and Fl anti-mu, as the latter population of cells is reported to lack surface IgD.

Age Factors↗
PubMed1976

Antibodies to nucleic acids in congenital immune deficiency states.

The presence of antibodies to native DNA, single-stranded DNA, and double-stranded RNA was determined for 37 patients with selective IgA deficiency, 11 patients with Wiskott-Aldrich syndrome, seven patients with common variable agammaglobulinemia, 14 patients with ataxia telangiectasia, six patients with intestinal lymphangiectasia, and one patient with Nezelof syndrome. Of 37 patients with selective IgA deficiency, 11 had antibodies to at least one nucleic acid; six had antibodies to native DNA, seven had antibodies to single-stranded DNA, and four had antibodies to double-stranded RNA. The only other congenital immune deficiency disease studied in which antibodies to nucleic acids were found was the Wiskott-Aldrich syndrome; in this group three of 11 patients had antibodies to native DNA. Retrospective analysis of our patients with SLE disclosed a 2.6% prevalence of IgA deficiency, a prevalence clearly higher than in the general population. These studies provide further evidence of the association between autoimmunity and abnormalities of IgA production and suggest a relationship between thymic-derived immune regulation and IgA production.

Adult↗
PubMed1976

Characterization of lymphocyte inhibition by supernatants of crowded lymphocytoblasts.

Crowded lymphocytoblasts produce a factor (or factors) that inhibits the response of peripheral blood lymphocytes to mitogens. This factor is destroyed by pepsin in 1 hr but not by neuraminidase. No activity was lost when the factor was incubated with packed human red blood cells, human lymphocytes, mouse spleen cells, or tissue culture cells. An antiserum was made to the factor which was capable of partially inhibiting its activity. The factor is active at about 25 mug/ml of protein. Maximal inhibition occurs if the factor is present for the duration of the culture period. This factor may play a regulatory role in the immune response.

Cell Line↗
PubMed1976

A human cold agglutinin which binds lacto-N-neotetraose.

A human cold agglutinin (McC) has been isolated from the serum of a patient with Waldenström's macroglobulinemia by affinity chromatography with a column of glutaraldehyde-fixed erythrocyte stroma mixed with celite. The agglutinin, which is an IgM K, reacts weakly with normal adult erythrocytes and strongly with cord cells as well as with adult Oh and Oi cells. The reactivity of all cell types tested was increased to approximately the same level by treatment of the cells with ficin. Inhibition studies indicate the agglutinin is specific for the nonreducing terminal carbohydrate sequence Gal(beta)1-4GlcNAc(beta)1-3Gal.

ABO Blood-Group System↗
PubMed1976

Selective inhibition of lymphocyte responsiveness to phytohaemagglutinin in patients with Reiter's syndrome.

The influence of synovial fluid from four patients with Reiter's syndrome on lymphocyte responsiveness was studied. On synovial fluid was found which specifically depressed the responsiveness of lymphocytes from patients with Reiter's syndrome to the non-specific mitogen phytohaemagglutinin (PHA). The ratio of the responsiveness of lymphocytes cultured in the presence of foetal calf serum (FCS), compared to those incubated in the Reiter's synovial fluid, was used as a measure of the depression induced by the Reiter's synovial fluid. The mean ratio for eight normals stimulated with PHA was 0-70 (range 0-35-0-96), while for eight patients with Reiter's syndrome, it was 0-13 (range 0-07-0-19). Similar studies done with concanavalin A (con A) showed no difference between lymphocytes from normals (0-73) or patients with Reiter's syndrome (0-67). Chromatography of the Reiter's synovial fluid on a Sepharose 4-B column resulted in the separation of three major fractions, one of which exhibited the inhibitory activity. When this active fraction was absorbed with Reiter's lymphocytes, a loss of the inhibitory activity of the fraction was seen. A similar absorption with normal lymphocytes had no effect. These studies demonstrate that a factor present in the synovial fluid of a patient with Reiter's syndrome reacted specifically with lymphocytes from patients with Reiter's disease and not with lymphocytes from normals. The interaction of this factor with lymphocytes from patients with Reiter's syndrome inhibited the responsiveness of these lymphocytes to PHA but not to con A.

Adult↗
PubMed1975

The development of anti-immunoglobulin antibodies in rhesus monkeys repeatedly exposed to Schistosoma japonicum.

The development of anti-immunoglobulin (Ig) antibodies in rhesus monkeys repeatedly exposed to Schistosoma japonicum cercariae was studied. Anti-Ig developed in all 8 monkeys exposed 5 times to cercariae of the Formosan strain, while none of 4 monkeys exposed once to the Philippine strain developed such antibodies in the same period. All monkeys developing anti-Ig had specificities for IgA, 6 of 8 for IgM and IgG, and 7 of 8 for rabbit Ig. The persistence of anti-Ig was greatly extended in the monkeys exposed initially to the Formosan strain and then challenged with the Philippine strain. A single monkey exposed once to the Philippine strain developed anti-IgA and anti-rabbit Ig 85 weeks postinfection. No relationship between host reaction to trapped eggs and the development of anti-Ig was discerned. The results suggest that immunization protocols designed for humans be carefully examined for their potential immunopathological side effects.

Animals↗
PubMed1975

Immune response of guinea pigs to Schistosoma mansoni. I. In vitro effects of antibody and neutrophils, eosinophils and macrophages on schistosomula.

Schistosomula of Schistosoma mansoni were rapidly killed in vitro by IgG2 antibodies from serum of schistosome-infected guinea pigs and heat-labile factors present in normal serum. Addition of polymorphonuclear neutrophilic leukocytes greatly increased the rate and degree of killing. Eosinophils and macrophages did not increase the level of killing, though they did react with schistosomula already damaged or killed by antiserum. Neutrophils and eosinophils reacted with schistosomula only in the presence of specific antibody, while macrophages nonspecifically attacked dead schistosomula. Serum antibody levels reached a plateau at approximately 6 weeks after a single infection. Attempts to precoat schistosomula with antibody prior to exposure to complement were largely unsuccessful.

Animals↗
PubMed1974

Demonstration of a blocking factor in the plasma and spinal fluid of patients with subacute sclerosing panencephalitis. I. Partial characterization.

Conflicting reports on the immune responsiveness of patients with subacute sclerosing panencephalitis (SSPE) have been reported. This report shows that the leucocytes from four SSPE patients exhibited strong sensitivity to both measles and SSPE virus preparations as measured by the macrophage migration inhibition test, mixed lymphocyte virus infected cell culture test, and the lymphotoxin assay. Earlier suggestions that a factor may be operating to suppress cellular reactivity are confirmed by the demonstration that the response of lymphocytes from SSPE patients could be blocked by the addition of SSPE spinal fluid or plasma. It was determined that the blocking factor was stable at -20 degrees C, heat labile at 56 degrees C for 30 minutes, trypsin and neuraminadase sensitive, and had a mol wt greater than 150,000 as determined by Sephadex G-200 gel chromatography. The blocking factor appeared to be specific for SSPE virus and did not block the response of lymphocytes to nonspecific mitogenic agents and other viral and bacterial agents.

Antibodies↗