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Scandinavian journal of immunology1980; 11(1); 53-62; doi: 10.1111/j.1365-3083.1980.tb00208.x

A primary immune response to dextran B512 is followed by a period of antigen-specific immunosuppression caused by autoanti-idiotypic antibodies.

Abstract: After a primary immune response to the alpha 1-6 epitope of dextran B512, dextran high responder strains exhibit a specific inability to produce IgM and IgG antibodies against this epitope, although they gave an expected secondary response to horse erythrocytes. Spleen cells from dextran-primed and-suppressed mice responded well to dextran after transfer to lethally irradiated previously untreated mice, indicating that tolerance or exhaustive proliferation of dextran reactive B cells is not responsible. Thymus-dependent dextran-protein conjugates also induced specific suppression. Suppression to both dextran and horse erythrocytes could be passively transferred into untreated recipients with immune serum. However, after absorption with horse erythrocytes and dextran, passive serum transfer only suppressed the response to dextran. It is suggested that the specific immunosuppression was caused by the appearance of autoanti-idiotypic antibodies directed against the immunoglobulin receptors of dextran-reactive B cells.
Publication Date: 1980-01-01 PubMed ID: 9537029DOI: 10.1111/j.1365-3083.1980.tb00208.xGoogle Scholar: Lookup
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  • Journal Article
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Summary

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The study examined the immunosuppression following a primary immune response to dextran B512, suggesting that this suppression is caused by autoanti-idiotypic antibodies, which interfere with the body’s immune response against certain antigens.

Understanding the Immune Response to Dextran B512

  • The research first discusses a primary immune response to Dextran B512. In individuals or strains that are high responders to dextran, an injection of dextran triggers an immune response where the body produces specific antibodies (IgM and IgG) against an epitope (part of an antigen that is recognized by the immune system) on dextran.
  • However, after this primary immune response, these high-responder strains showed a specific inability to produce the same antibodies against this dextran epitope. Interestingly, their immune response against other antigens, like horse erythrocytes (horse red blood cells) was unimpaired, indicating a specific immunity suppression to dextran.

Investigating the Cause of Immunosuppression

  • To investigate whether this inability to produce antibodies was due to tolerance or exhaustive proliferation of dextran reactive B cells, spleen cells from dextran-primed and suppressed mice were transferred into untreated mice that had been lethally irradiated. These transferred cells responded well to dextran, ruling out the possibility of tolerance or exhausted proliferation of reactive cells being the cause.
  • Additionally, the researchers found that the suppression could be transferred to other animals by injection of immune serum. However, if this serum was absorbed by horse erythrocytes and dextran, the transferred immunity only affected the response to the dextran. This finding reinforced their earlier assertions that this was a specific suppression targeted at dextran.
  • Based on these findings, the paper suggests that this immunosuppression is caused by the appearance of autoanti-idiotypic antibodies. These are antibodies produced by the body that recognize and bind to the idiotypes (unique sets of antigenic determinants) of the antibodies produced during the immune response. In this case, these autoimmune antibodies were directed against the immunoglobulin receptors of dextran-reactive B cells, effectively suppressing the immune response to dextran by preventing these cells from recognizing and responding to it.

Cite This Article

APA
Fernandez C, Möller G. (1980). A primary immune response to dextran B512 is followed by a period of antigen-specific immunosuppression caused by autoanti-idiotypic antibodies. Scand J Immunol, 11(1), 53-62. https://doi.org/10.1111/j.1365-3083.1980.tb00208.x

Publication

ISSN: 0300-9475
NlmUniqueID: 0323767
Country: England
Language: English
Volume: 11
Issue: 1
Pages: 53-62

Researcher Affiliations

Fernandez, C
  • Department of Immunobiology, Karolinska Institute, Stockholm, Sweden.
Möller, G

    MeSH Terms

    • Animals
    • Antibodies, Anti-Idiotypic / immunology
    • Antibody Formation
    • Autoantibodies / immunology
    • Dextrans / immunology
    • Erythrocytes / immunology
    • Horses
    • Immunoglobulin G / biosynthesis
    • Immunoglobulin M / biosynthesis
    • Immunologic Memory
    • Immunosuppression Therapy
    • Mice
    • Mice, Inbred C57BL
    • Mice, Inbred CBA

    Citations

    This article has been cited 3 times.
    1. Fernandez C, Mäkelä O, Möller G. Genetics of the anti-dextran B512 and the autoanti-idiotypic response: codominant expression in F1 hybrids and dichotomy of response and allotype-linked idiotype.. Immunogenetics 1980;10(6):573-82.
      doi: 10.1007/BF01572591pubmed: 22457936google scholar: lookup
    2. Sverremark E, Fernandez C. Immunogenicity of bacterial carbohydrates: cholera toxin modulates the immune response against dextran B512.. Immunology 1997 Sep;92(1):153-9.
    3. Möller G. Role of antigen and antibody in the regulation of the immune response.. Folia Microbiol (Praha) 1985;30(3):203-11.
      doi: 10.1007/BF02923512pubmed: 2408979google scholar: lookup