Genetic control of immune response to staphylococcal nuclease. XII: Analysis of nuclease antigenic determinants using anti-nuclease monoclonal antibodies

1985 ◽  
Vol 68 (1) ◽  
pp. 31-40 ◽  
Author(s):  
Christian A. Devaux ◽  
Paul I. Nadler ◽  
Geraldine G. Miller ◽  
David H. Sachs
Keyword(s):  
Immune Response ◽  
Monoclonal Antibodies ◽  
Genetic Control ◽  
Staphylococcal Nuclease ◽  
Antigenic Determinants

scholarly journals Genetic control of the immune response to staphylococcal nuclease. VII. Role of non-H-2-linked genes in the control of the anti-nuclease antibody response

1978 ◽  
Vol 147 (2) ◽  
pp. 396-408 ◽  
Author(s):  
DS Pisetsky ◽  
JA Berzofsky ◽  
DH Sachs
Keyword(s):  
Immune Response ◽  
Antibody Response ◽  
Genetic Control ◽  
Heavy Chain ◽  
Staphylococcal Nuclease ◽  
Antigenic Determinants ◽  
Structural Genes ◽  
Antibody Titers ◽  
Freund's Adjuvant

The role of non-H-2-linked genes in the control of the antibody response to staphylococcal nuclease has been investigated. 3 wk after immunization with nuclease in complete Freund's adjuvant, strain A/J (H-2 a) mice produced significantly higher titers of antibody than strain B10.A (H-2(a)) mice, whereas mice of strains A.BY (H-2(b)) and B10 (H-2(b)) produced barely detectable titers. With hyperimmunization, A/J and A.BY mice reached the same peak levels for antibody titers, both severalfold higher than those reached by B10.A and B10 mice. Analysis of the specificity of antibodies by assessment of binding to two fragments of nuclease showed similarities between strains of the same H-2 haplotype. These results suggest that although H-2-1inked genes determined initial responsiveness at 3 wk and the relative proportions of antibodies directed toward different antigenic determinants on the nuclease molecule, non-H-2-linked genes determined the overall magnitude of the hyperimmuneresponse. Measurement of the affinity of the antibodies to the nuclease fragment (1-126) showed that strains B10 and B10.A produced antibodies with 7- to 10-fold higher affinity than comparable antibodies from strains A.BY and A/J. In a backcross of (B10.A × A/J) × B10.A, the level of antibody segregated independently of the Ig-1(e) C(H) allotype and the A/J anti-nuclease idiotypes. Thus, a gene(s) linked to neither H-2 nor heavy chain structural genes appears to control the aggregate response to antigenic determinants on the nuclease molecule independent of subspecificities of these antibodies or their idiotype.

Genetic Control of the Immune Response to Staphylococcal Nuclease in Mice

1978 ◽  
pp. 241-257 ◽  
Author(s):  
Jay A. Berzofsky ◽  
David S. Pisetsky ◽  
Ronald H. Schwartz ◽  
Alan N. Schechter ◽  
David H. Sachs
Keyword(s):  
Immune Response ◽  
Genetic Control ◽  
Staphylococcal Nuclease

scholarly journals GENETIC CONTROL OF THE ANTIBODY RESPONSE

1967 ◽  
Vol 126 (5) ◽  
pp. 969-978 ◽  
Author(s):  
Hugh O. McDevitt ◽  
Michael Sela
Keyword(s):  
Immune Response ◽  
Antibody Response ◽  
Glutamic Acid ◽  
Genetic Control ◽  
Antigenic Determinants ◽  
Polyglutamic Acid ◽  
Cross Reactions ◽  
Cba Mice ◽  
Related Series ◽  
Synthetic Polypeptide

CBA and C57 mice were tested for their ability to make an immune response to a related series of branched, multichain synthetic polypeptide antigens in which the antigenic determinants on the amino termini of the branched side chains were systematically varied. Neither strain responded to the polyglutamic acid determinant. Both strains responded well and equally to the poly(phenylalanine, glutamic acid) determinants. CBA mice responded poorly, and C57 mice responded well to two different antigens bearing poly(tyrosine, glutamic acid) determinants. CBA mice responded well, and CS7 mice responded poorly to two different antigens bearing poly(histidine, glutamic acid) determinants. The genetic control of the immune response to (H,G)-A--L appears to be dominant and polygenic, as it has been shown to be for (T,G)-A--L. The related antigens used in this study show extensive cross-reactions with antisera against other members of the related series.

scholarly journals The analysis of the monoclonal immune response to influenza virus. II. The antigenicity of the viral hemagglutinin.

1976 ◽  
Vol 144 (4) ◽  
pp. 985-995 ◽  
Author(s):  
W Gerhard
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Monoclonal Antibodies ◽  
Influenza Viruses ◽  
Antigenic Determinants ◽  
Humoral Immune ◽  
Viral Hemagglutinin ◽  
Or Groups ◽  
Virus Strains

The antigenicity of the hemagglutinins (HA) of five influenza viruses of the A0 and A1 subtypes has been analyzed by means of monoclonal antibodies of murine origin produced in vitro. Secondary monoclonal anti-HA(PR8) antibodies were able to differentiate 14 antigenic determinants (or groups of determinants) on the HA of five influenza virus strains of the A0 and A1 subtypes. Taking into account that certain pairs of determinants delineated on heterologous HA may reflect the heterogeneity of the humoral immune response to a single homologous determinant, the presence of at least eight determinants (host cell-derived determinants not included) on the homologous HA of PR8 and probably on the HA of influenza viruses in general is postulated. Three types of HA-determinants of A0 and A1 influenza virus strains could be distinguished: strain-specific, partially shared, and determinant(s) common to all five virus strains tested. Roughly 40, 55, and 5%, respectively, of the secondary anti-PR8 antibodies of BALB/c mice were directed against determinants belonging to either of the three types.

Genetic control of the immune response to staphylococcal nuclease

1984 ◽  
Vol 60 (2) ◽  
pp. 137-145 ◽  
Author(s):  
Geraldine P. G. Miller ◽  
David H. Sachs
Keyword(s):  
Immune Response ◽  
Genetic Control ◽  
Staphylococcal Nuclease

Genetic control of the immune response to staphylococcal nuclease

1978 ◽  
Vol 1 (1) ◽  
pp. 51-83 ◽  
Author(s):  
David H. Sachs ◽  
Jay A. Berzofsky ◽  
David S. Pisetsky ◽  
Ronald H. Schwartz
Keyword(s):  
Immune Response ◽  
Genetic Control ◽  
Staphylococcal Nuclease
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