Modulation of the H‐2 Antigenicity on the Surface of Murine Peritoneal Cells

and are most likely explained by the appearance of a new cell clone [32,33]. These data will be published separately.Phenotypic linkage to the allotype of H-chains and the individuality of kinetic properties can be interpreted in two ways: (a) all mice share the same gene pool, but selection from the pool is on an individual basis; (b) mice differ in the repertoire of their variable genes by a mechanism of somatic variability. In any case, somatic selection or somatic variability operate on the level of each chromosome characterized by allotype in heterozygous animals.The experiments reported here did not take into consideration the fact that our allotype antisera react with determinants on two IgG subclasses: IgGl and IgG2a [ 111. Experiments to analyze these subclasses separately have been done [ 191. They show that subclasses belonging to the same allelic group (i.e., determined in their constant parts by loci on the same chromosome) are highly correlated in their kinetic properties [34]. We are greatly indebted to Pro8 Charles Steinberg of the Basel Institute for Immunology for his collaboration in the theoretical aspects of this work, and to Mr. HamAlbert K d b of this university, for aiding us in mathemtical analysis of the &a. Pro$ N. Zuber, ETH ZUrich, kindly performed the amino acid analyses of alanylated p r e teins.The capacity of macrophage components to inhibit anti-macro phage serum activity Anti-macrophage serum (AMS) was shown to lose part of its activity after incubation with macrophages. Both the cytotoxic and phagocytic inhibition properties of AMS decreased significantly after 12 h incubation with macrophages.Free and/or AMS-bound macrophage antigens were found t o be shed from the cell surface into the culhre medium during incubation of macrophages with AMS.Labeled macrophage components were demonstrated to bind specifically to AMS, suggesting that the loss of AMS activity was mainly due to the blocking of antimacrophage antibody combining sites by macrophage antigens.

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The capacity of macrophage components to inhibit anti‐macrophage serum activity

Schroit

Geiger

Gallily

1973

Eur J Immunol

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Antibody‐induced changes in expression of the H‐2 antigen

Lesley

Hyman

1974

Eur J Immunol

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Continuous exposure of a BALB/c myeloma line to anti‐H‐2d antibody in the absence of complement, for 3 hours at 37 °C, results in the loss of sensitivity to lysis by added complement or by added anti‐H‐2d and complement (antigenic modulation). 125I‐labeled anti‐H‐2d was used to follow the fate of the modulating antibody. Iodinated rabbit anti‐mouse Ig was used to detect anti‐H‐2 Ig remaining on the cell surface at various times. It was found that the amount of anti‐H‐2 antibody detectable on the cell surface decreases by 1/3 to 1/2, and that this decrease occurs by internalization of the bound antibody (and presumably of the antigen). Maintenance of antigenic modulation over a 24‐hour period involves a steady state of continuous binding of free antibody and its internalization. Recovery from antigenic modulation occurs during 3 hours after removal of the anti‐H‐2 antibody and involves a decrease in the amount of mouse anti‐H‐2d remaining on the cell surface (as detected by labeled rabbit anti‐mouse Ig) and an increase in the amount of surface antigen detected by the ability to bind 125I‐labeled anti‐H‐2d.

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The association of H‐2 antigens and EAC receptors on the surface of peritoneal cells

Schlesinger

Chaouat

1975

Eur J Immunol

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The exposure of murine peritoneal cells to anti-H-2 sera results in a diminished expression of H-2 antigen on the cell surface. Concomitant with this "H-2 modulation" the capacity of macrophages to bind sheep red blood cells coated with antibody and complement (EAC) was markedly diminished. In contrast, there was no change in the capacity of modulated macrophages to bind sheep red blood cells coated with antibody alone (EA). Antibodies to K end H-2 specificities were more effective in reducing the binding of EAC than antibodies to D end H-2 specificities. Exposure of peritoneal cells to O or Ly antisera had no effect on the formation of EAC rosettes. Exposure of peritoneal cells to anti-H-2 sera, under conditions which would not allow modulation of H-2 antigens, also prevented the reduction of EAC binding. Thus, the EAC receptors and H-2 antigenic specificities seem to be closely related on the surface of peritoneal cells, but constitute distinct cell surface structures. Preliminary evidence indicates that vinblastine, a microtubule depolymerizing agent, may disrupt the close association of EAC receptors and H-2 antigens. It is suggested that the association of EAC receptors and K end H-2 determinants on the membrane of macrophages may have implications for the regulation of the immune response by H-2-linked Ir genes.

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Modulation of the H‐2 Antigenicity on the Surface of Murine Peritoneal Cells

Cited by 25 publications

References 14 publications

The capacity of macrophage components to inhibit anti‐macrophage serum activity

The capacity of macrophage components to inhibit anti‐macrophage serum activity

Antibody‐induced changes in expression of the H‐2 antigen

The association of H‐2 antigens and EAC receptors on the surface of peritoneal cells

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