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Biomedical subjects

B C Gilliland

Publications and source records attributed to B C Gilliland.

At least 19 recordsLinked to original sources
PubMed1987

The limited spectrum of antinuclear antibodies in leprosy.

Sera from 46 consecutive patients with leprosy were collected and tested against an extensive panel of defined nuclear antigens. Antinuclear antibodies (ANA) were present in 16% of patients, but the titer was uniformly low and there was no consistent fluorescence pattern. None of the ANA positive sera contained antibodies which reacted with native DNA, or which were directed against histones, centromeres, SSB, Sm, or ribonucleoprotein. These more specific autoantibody assays thus retained their clinical utility in the differential diagnosis of rheumatologic complaints in patients with leprosy.

Adolescent↗
PubMed1979

Detection of intermediate complexes by evaluation of the difference between gamma-globulin and IgG concentrations.

A simple analysis based on techniques readily available in the routine clinical laboratory has been presented for identification of patients with moderate and high levels of intermediate complexes. If the gamma-globulin concentration determined by serum protein electrophoresis minus the IgG concentration determined by radial immunodiffusion exceeds 1.0 gm/dl, intermediate complexes of IgG should be present in concentrations greater than 0.5 gm/dl. In principle, any disease association with sufficient polymerization of IgG might cause an abnormal result with this analysis. Furthermore, sera from patients with liver disease and marked beta-gamma-bridging on electrophoresis may also give abnormal values.

Arthritis, Rheumatoid↗
PubMed1978

Synthesis by an established lymphocyte cell line from a rheumatoid synovium.

Lymphocytes derived from the synovium of a patient with rheumatoid arthritis were shown to synthesize predominantly IgG as measured by an equilibrium binding assay. Chromatographic separation of the radiolabeled lymphocyte culture supernatant revealed rheumatoid factor activity associated with IgG and IgM. In addition, immunofluorescence studies on fixed lymphocytes demonstrated that the majority of cells stained positive for both IgG and rheumatoid factor.

Arthritis, Rheumatoid↗
PubMed1978

Effect of immunization on susceptibility to experimental Streptococcus mutans and Streptococcus sanguis endocarditis.

It has been asserted that humoral immunity is an important potentiating factor in pathogenesis of infective endocarditis, in that prior immunization to certain bacteria may predispose the host to endocarditis caused by those organisms. If so, possible future vaccination of humans with streptococcal antigens for the prevention of dental caries might increase the susceptibility of the population to streptococcal endocarditis. To examine this hypothesis further, we immunized rabbits with killed Streptococcus sanguis or Streptococcus mutans. After complement-fixing antibody had developed, the rabbits were tested for susceptibility to experimental infective endocarditis. Rabbits with high titers of complement-fixing antibody to the infecting organism developed streptococcal endocarditis less often (13%) than animals with lower titers (69%; P less than 0.0002). These findings do not support the hypothesis that pre-immunization predisposes to infective endocarditis and lend no credence to the concept that vaccination of human subjects against dental caries might increase their susceptibility to streptococcal endocarditis. On the contrary, the results of these experiments indicate that specific antibody can confer relative immunity to infective endocarditis.

Animals↗
PubMed1977

Linkage between the gene (or genes) controlling synthesis of the fourth component of complement and the major histocompatibility complex.

In an attempt to map the gene (or genes) controlling the synthesis fo the fourth component of complement (C4), we performed linkage studies in a family with hereditary C4 deficiency. The proband, a seven-year-old boy with lupus erythematosus, consistently lacked deteftable serum C4 by both functional and protein measurements. The complement defect was transmitted as an autosomal recessive disorder. Eight of 15 family members were considered to be heterozygotes, seven because of low C4 levels and one because of genetic data (obligate heterozygote). The gene (or genes) coding for C4 deficiency appeared to be linked to the major histocompatibility complex (A2,B12,DW2 on the maternal side and A2,BW15,LD108 on the paternal side) and to other markers known to be in close proximity to the histocompatibility complex on chromosome 6 (phosphoglucomutase-3, glyoxalase-1 and properdin factor B).

Child, Preschool↗
PubMed1977

Immunologic quantitation of serum immunoglobulins.

The methods available in the clinical laboratory for measuring serum immunoglobulins (G, A, M, and D) include radial immunodiffusion, electroimmunodiffusion and nephelometry. All these immunochemical technics require specific antisera and stable standards for reproducible and accurate results. Discrepancies between the quantity of protein measured by any of these technics and the actual chemically or physically measured quantity arise when the unknown and standard differ in molecular size, electrophoretic mobility, or antigenic valence. These differences may lead to over- or under-estimation of the quantity of immunoglobulin. Quantitation of immunoglobulins, especially in context with protein electrophoresis, does provide useful information for diagnosis and treatment of selective disorders.

Adolescent↗
PubMed1976

Coombs--negative immune hemolytic anemia.

An immune hemolytic anemia occurs in a few patients in whom the concentration of antibody on the red cell is below the level for detection by the usual antiglobulin test. Clinically, these patients are identical to patients with warm type Coombs-positive hemolytic anemia, except for the quantity of antibody on the cell. The course of the hemolytic disease is highly variable. It is postulated that the properties of the antibody in conjunction with the sensitivity of the reticuloendothelial system for antibody-coated cells account for hemolytic anemia occurring with such low concentrations of antibody. The response to steroid therapy and splenectomy, when indicated, is usually favorable.

Anemia, Hemolytic, Autoimmune↗
PubMed1971

Studies on antigen-antibody complexes. I. Elimination of soluble complexes from rabbit circulation.

Solid phase immunoadsorbents were prepared by coupling antigens to agarose. With this technique specific antibodies were easily isolated in large amounts. The gammaG-globulin class of antibodies isolated in this manner were not denatured as judged by their normal biological half-life in rabbits. Soluble immune complexes at fivefold antigen excess were prepared from isolated specific antibodies and HSA, human lambda-chains, human lambdaG-globulins, and a Waldenström's macroglobulin as antigens. In all these preparations a characteristic immune complex was encountered that represented the smallest stable antigen-antibody union. In the HSA-anti-HSA system they were found to be AgAb(2) complexes, and Ag(2)Ab complexes in the gammaG-anti-gammaG system. These stable complexes fixed complement ineffectively. Also, a spectrum of larger complexes was present in each system, and these complexes fixed complement effectively. With intact antibodies the disappearance curves of immune complexes from the circulation were composed of three exponential components. The immune complexes larger than AgAb(2) were quickly removed from the circulation with half-lives of 0.09-0.37 hr. Their clearance was not dependent on complement components, in that depletion of complement by cobra venom factor and aggregated gammaG-globulin did not alter the pattern of their removal from the circulation. However, when the interchain disulfide bonds of antibodies were reduced and alkylated, the removal of the lambda-anti-lambda, HSA-anti-HSA, and gammaG-anti-gammaG complexes was altered. In these experiments the disappearance curves were composed of two exponential components and the rapid removal of the greater than AgAb(2) complexes did not occur. The immune complexes prepared from reduced and alkylated antibodies fixed complement ineffectively. The presented data indicate that the rapid removal of circulating immune complexes, containing gammaG-globulin molecules as antibodies, depends primarily on the number of antibodies involved. Furthermore, complement fixation is not involved in the rapid removal of such complexes. Nevertheless, the rapid removal of immune complexes and their ability to fix complement have similarities for optimal function in that both processes require intact interchain disulfide bonds of antibodies and complexes that exceed the AgAb(2) combination.

Adsorption↗
PubMed1970

The detection of cell-bound antibody on complement-coated human red cells.

This study sought to elucidate the mechanism by which human red cells, in a variety of clinical settings, become coated in vivo with autologous complement components in the absence of anti-red cell autoantibodies demonstrable by standard methods. By means of a newly developed complement-fixing antibody consumption test, previously undetectable red cell-bound gammaG globulin could be detected and quantified. By this technique, the complement-coated red cells of 13 of 16 patients were shown to carry abnormally high numbers of gammaG molecules per cell, which were nevertheless below the level for detection by the direct antiglobulin test. Eluates were made from the red cells of seven of these patients and each eluate, when sufficiently concentrated, was capable of sensitizing normal human red cells (with gammaG antibodies) to give a positive indirect antiglobulin test with anti-gammaG serum. In the presence of fresh normal serum, six of the eluates so tested were capable of fixing complement to normal human red cells. The antibodies in the red cell eluates did not exhibit Rh specificity and did not react with nonprimate red cells. When studied by sucrose gradient ultracentrifugation, the gammaG antibodies to human red cells in these eluates sedimented in the 7S region. It is concluded that in many patients in whom direct antiglobulin tests reveal only cell-bound complement, the complement fixation is mediated in vivo by small quantities of "warm-reacting" erythrocyte autoantibodies of the gammaG class.

Animals↗