Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1959 Jan;2(1):31-43.

The mechanism of anaphylaxis: specificity of antigen-induced mast cell damage in anaphylaxis in the guinea pig

The mechanism of anaphylaxis: specificity of antigen-induced mast cell damage in anaphylaxis in the guinea pig

J H HUMPHREY et al. Immunology. 1959 Jan.

Abstract

Mast cell damage, characterized by loss of granules, occurs when the tissues of sensitized guinea pigs are brought into contact with antigen in vivo or in vitro. Quantitative studies on the mesenteries of passively sensitized guinea pigs show that the mast cell response to antigen is well correlated with the development of anaphylactic shock. After multiple sensitization contact with different antigens caused cumulative, but not complete, disappearance of mast cells.

Antigen-antibody interactions, in which antisera were from species which do not sensitize guinea pigs passively for anaphylaxis, did not cause mast cell damage.

Reversed passive anaphylaxis and mast cell damage were elicited when the antigen was a suitable γ-globulin, but not an albumin. Antiserum against homologous γ-globulin causes typical anaphylaxis and mast cell degranulation, whereas antiserum against Forssman antigen causes capillary damage without mast cell changes, and antiserum against homologous albumin is ineffective.

These findings can be explained by the hypothesis that mast cell damage occurs as a result of antigen-antibody interaction, when one of the reagents is reversibly adsorbed at the mast cell surface, and when they are together capable of activating some process or agent whose further action depends upon the metabolic integrity of the cells.

PubMed Disclaimer

References

    1. J Physiol. 1953 Jun 29;120(4):528-37 - PubMed
    1. Proc Soc Exp Biol Med. 1955 Oct;90(1):303-4 - PubMed
    1. J Physiol. 1956 Jan 27;131(1):207-19 - PubMed
    1. Nature. 1956 Mar 3;177(4505):427-9 - PubMed
    1. J Immunol. 1956 Sep;77(3):198-212 - PubMed

LinkOut - more resources