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Biomedical subjects

R P Messner

Publications and source records attributed to R P Messner.

At least 109 records · Page 6Linked to original sources

Receptors for human gamma G globulin on human neutrophils.

Cell surface receptors for human gammaG antibodies directed against bacterial antigens were demonstrated on human neutrophils using an in vitro bacteriocidal-phagocytic assay. These results were confirmed by adherence of sensitized erythrocytes to monolayers of neutrophils or monocytes. Erythrocytes sensitized indirectly with antibacterial gammaG antibodies after passive sensitization with bacterial antigens adhered to both neutrophils and monocytes. Erythrocytes sensitized directly with conventional anti-D gammaG antibodies adhered only to monocytes, while those sensitized with the hyperimmune anti-CD gammaG antibody Ripley adhered to both monocytes and neutrophils. Adherence of anti-Rh or antibacterial gammaG antibodies to monocytes and neutrophils could be inhibited by whole gammaG, myeloma globulins of the gamma(1) or gamma(3) subclasses, or Fc fragments, but not by Fab fragment. These results indicate that receptors for the Fc portion of human gammaG antibodies exist on both neutrophils and monocytes, and that gammaG antibodies differ in their ability to attach to these two cell types. Differences in the behavior of the gammaG antibodies studied may be related to differences in the density of antibodies on the erythrocyte surface and receptors on the phagocytic cells.

Antigen-Antibody Reactions↗

Phagocytosis in subacute bacterial endocarditis. Localization of the primary opsonic site to Fc fragment.

The opsonic properties of immune gammaG-globulins isolated from patients with chronic septicemic conditions, principally subacute bacterial endocarditis were studied. Opsonic capacity as well as complement-fixing properties of gamma-globulins appeared to be closely associated with integrity of Fc structures. Progressive pepsin digestion of immune gammaG-globulins, as monitored by successive loss of Gm(a) and Gm(b) antigens, abolished opsonic activity. Colostral gammaA, containing agglutinating antibacterial antibodies but no demonstrable complement-fixing activity, was devoid of opsonic capacity. Reduction of gamma-globulin opsonins with 0.01 or 0.1 M mercaptoethanol progressively abolished opsonic activity in parallel with loss of ability of treated gamma-globulins to fix complement with bacteria. Treatment of gamma-globulin opsonins with 0.01 M sodium metaperiodate also produced complete loss of opsonic capacity in parallel with loss of Gm(b) Fc antigens. These findings, together with antiopsonic effects demonstrable with anti-gamma-globulin factors showing primary reactivity with Fc structures, indicate that the opsonic property of immune gamma-globulins requires the participation of structures integral to the Fc region of gamma-globulin.

Agglutination Tests↗

Serum opsonin, bacteria, and polymorphonuclear leukocyte interactions in subacute bacterial endocarditis. Anti-gamma-globulin factors and their interaction with specific opsonins.

The effect of anti-gamma-globulin factors on 7S gamma-globulin opsonins from patients with subacute bacterial endocarditis has been examined with a quantitative in vitro phagocytosis system. Human anti-gamma-globulin factors from patients with subacute bacterial endocarditis and rheumatoid arthritis inhibited the opsonic action of 7S gamma-globulin specifically bound to bacteria. A similar antiopsonic effect was obtained with rabbit antiserum to human gammaG globulin. The antiopsonic effect of anti-gamma-globulin factors did not correlate with their ability to potentiate agglutination of bacteria by 7S antibody. Competition was demonstrated between the antiopsonic effect of anti-gamma-globulin factors and the phagocytosis-promoting action of heat-labile serum factors containing hemolytically active complement.

Agglutination Tests↗