Publications by authors named "Winchester R"

Direct immunofluorescence performed with the F(ab)2 fragment of rabbit antibodies to IgG revealed that membrane bound IgG was only rarely found on the surface of small peripheral blood lymphocytes (PBL). In contrast whole antibodies to IgG used in fluorescence gave much higher levels of cells with IgG surface staining. This staining resulted from secondary IgG binding, in part due to the uptake of newly formed immune complexes.

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A group of alloantibodies are found in pregnancy sera which react with antigens present on B lymphocytes and monocytes but are not detectable on the vast majority of unstimulated T cells. This specificity distinguishes them from HL-A antibodies which react with both cell types. They were readily recognized through indirect fluorescent antibody analysis by employing the combination of B-cell lymphoid lines and normal peripheral blood T cells.

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Antibodies to surface determinants of human lymphocytes, recognized both by cytotoxicity of fluorescent antibody analysis, were shown to be specifically enriched over the serum levels in cryoprecipitates from patients with systemic lupus erythematosus (SLE). The antilymphocyte antibody was shown to be cold reactive and was exclusively IgM. It was distinct from IgM anti-IgG, which was also variably concentrated in the cryoprecipitates.

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Anti-lymphocyte antibodies have been demonstrated in patients with SLE and RA by immunofluorescence. They differ from those arising through iso-immunization by being cold reactive and chiefly of the IgM class. Separate anti specificities were shown for determinants on either T or B cells.

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Early study of kindreds with C2 deficiency indicated that absence of C2 had no detrimental effect on affected individuals. Studies of additional kindreds, however, show a high incidence of SLE and other connective tissue diseases among homozygous C2-deficient members. A group of patients with an unusual SLE-related syndrome is described.

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Certain cases of chronic lymphocytic leukemia possess monoclonal bands in the serum. Idiotypic antibodies to the isolated IgM protein of one such case demonstrated that the leukemic lymphocytes carried the identical specificity on their lymphocytes. Both the lymphocyte IgM and the IgD possessed this same specificity.

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Brief digestion of human peripheral blood lymphocytes by vibrio cholera neuraminidase (VCN) revealed hidden components of the membrane. Autologous human serums contained antibodies directed to these components that were readily demonstrated by immunofluorescence. Antibodies of similar specificity were found in all normal serums.

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Antilymphocyte antibodies in serum from patients with systemic lupus erythematosus (SLE), as detected by microcytotoxicity and indirect immunofluorescence, were predominantly cold reactive and of the IgM class. These IgM antibodies were most active at 4 degrees C. IgG antibodies were infrequent, and were only minimally lymphocytotoxic.

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Certain cases of chronic lymphocytic leukemia are associated with monoclonal immunoglobulins in the serum. In the present study it was possible to demonstrate that the surface immunoglobulin of the leukemic lymphocytes was idiotypically identical to the serum monoclonal immunoglobulin of the same individual. This was done through the use of fluorescent antibodies that were prepared against the isolated immunoglobulin M kappa serum protein from patient Ei.

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Large percentages of the lymphocytes from some patients with rheumatoid arthritis and systemic lupus erythematosus were densely covered with Ig demonstrable by immunofluorescence, which was occasionally present in the form of caps. The amount and character of the Ig staining depended largely on the procedures used in the isolation and washing of the lymphocytes. Cold-reactive antilymphocyte antibodies present in many sera wre primarily responsible for these variations.

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Human sera were found to contain factors that stimulate and factors that inhibit porphyrin formation by cultured avian liver cells. The capacity of sera to stimulate or inhibit porphyrin formation varied in different hormonal states and in the porphyrias. Sera from 31 post partum women, eight of whom were not lactating, inhibited porphyrin formation to a mean level 30% below the level in control cultures and also inhibited drug and steroid stimulation of porphyrin formation.

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An analysis was made of the immunoglobulin surface markers of the cells of patients with chronic lymphatic leukemia (CLL) in view of previous evidence of their monoclonal B-cell character. The simultaneous presence of IgM and IgD on the surface of the majority of lymphocytes was demonstrated by both immunofluorescence and hemagglutination inhibition in most cases. However, cases were observed with surface IgM without IgD as well as cases with IgD without IgM.

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A marked homogeneity of the light chains was observed in an analysis of 17 IgM proteins with anti-gamma-globulin activity. The V region subgroups of the light chains were determined by both sequence and antigenic analysis. The latter procedure permitted large scale screening for comparisons with control proteins.

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Through the use of absorbed idiotypic antisera prepared against single isolated monoclonal IgM anti-gamma-globulins, partial cross-idiotypic specificity was demonstrated with other IgM anti-gamma-globulins. Such antisera classified these proteins into at least three groups. The major group which included 60% of the anti-gamma-globulins was particularly homogeneous.

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Single-stranded DNA (SDNA) occurs in high incidence and in greatest concentration in the sera of patients with systemic lupus erythematosus (SLE), where levels as high as 250 mug/ml were observed. SDNA appears to be an imunogen for anti-SDNA antibodies and forms complexes in vivo of both anti-SDNA-SDNA and anti-NDNA-SDNA types, which apparently play a role in the pathogenesis of the glomerulonephritis found in patients with SLE, SDNA is also found in high incidence but at lower levels in the sera of patients with rheumatoid arthritis. Lesser amounts of SDNA are found in several other diseases in which a low incidence of anti-SDNA antibodies is observed.

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gammaG globulin complexed in an unusual form has been demonstrated in the serum of many patients with rheumatoid arthritis. Such complexes have been detected and isolated principally through precipitation reactions with monoclonal gammaM rheumatoid factors. These monoclonal rheumatoid factors exhibited a greater sensitivity to react with small complexes or aggregates of gamma-globulin than polyclonal rheumatoid factor from rheumatoid arthritis sera or isolated C1q.

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Precipitin reactions of C1q in gel diffusion proved useful in detecting unknown complexes containing gamma-globulin in the sera of patients with SLE. Using this method low molecular weight C1q reactants also have been detected in a number of sera from patients with SLE as well as other diseases. Both the circulating complexes and the unidentified low molecular weight reactants are associated with disease activity and in vivo complement depression.

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