IgE-Dependent Release of Inflammatory Mediators from Hamster Mast Cells in Vitro

  • Timothy J. Sullivan
  • David A. Hart
  • J. Wayne Streilein
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 134)


The release of mediators from mast cells is an essential step in immediate hypersensitivity reactions and also appears to play a significant role in delayed hypersensitivity and some forms of complement mediated reactions (1). Mediator release from rat or human mast cells can be provoked by antigen-IgE interactions on the surface of cells, by C3a or C5a anaphylatoxins, by bradykinin, by basic lysosomal proteins from neutrophils, by certain lymphokines and by a variety of other molecules (1–4). Preformed molecules such as histamine and newly formed molecules such as slow reacting substance-A (SRS-A) and prostaglandin D2 (PGD2) are released which exert potent regulatory influences on tissue function in areas of mast cell secretion. In addition to roles in the effector arms of immune and non-specific inflammation, recent evidence indicates that mast cell mediators may exert important regulatory influences on the evolution of immune responses (5). While the precise roles of mast cells in these immunologic events are not entirely clear, it seems likely that important roles will be delineated in several areas of immune function.


Mast Cell Apparent Molecular Weight Mediator Release Human Mast Cell Mast Cell Secretion 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Sullivan, T.J.; Parker, C.W. Am J Pathol 85 (1976) 437.PubMedGoogle Scholar
  2. 2.
    Johnson, A.R. et al. Immunology 28 (1975) 1067.PubMedGoogle Scholar
  3. 3.
    Johnson, A.R.; Erdos, E.G. Proc Soc Exp Biol Med 142 (1973) 1252.PubMedGoogle Scholar
  4. 4.
    Seegers, W.; Janoff, A. J Exp Med 124 (1966) 833.PubMedCrossRefGoogle Scholar
  5. 5.
    Plaut, M. J Allergy Clin Immunol 63 (1979) 371.PubMedCrossRefGoogle Scholar
  6. 6.
    Hook, W.A. et al. Infect Immun 2 (1970) 462.PubMedGoogle Scholar
  7. 7.
    Hook, W.A. et al. Infect Immun 9 (1974) 903.PubMedGoogle Scholar
  8. 8.
    Boreus, L.O. Acta Physiol Scand 49 (1960) 251.PubMedCrossRefGoogle Scholar
  9. 9.
    Keller, R. Int Arch Allergy 34 (1968) 139.PubMedCrossRefGoogle Scholar
  10. 10.
    Sullivan, T.J. et al. J Immunol 117 (1976) 713.PubMedGoogle Scholar
  11. 11.
    Sullivan, T.J. et al. J Immunol 114 (1975) 1473.PubMedGoogle Scholar
  12. 12.
    Marquardt, D.L. et al. J Immunol 120 (1978) 871.PubMedGoogle Scholar
  13. 13.
    Eidels, L. et al. Mol Immunol 16 (1979) 541.PubMedCrossRefGoogle Scholar
  14. 14.
    Bray, R.E.; Arsdel, P.P. Proc Soc Exp Biol Med 106 (1961) 255.Google Scholar
  15. 15.
    Snyder, S.H. et al. J Pharmacol Exp Ther 153 (1966) 544.PubMedGoogle Scholar
  16. 16.
    Kulczycki, A. Jr. et al. J Biol Chem 254 (1979) 3194.PubMedGoogle Scholar

Copyright information

© Plenum Press, New York 1981

Authors and Affiliations

  • Timothy J. Sullivan
    • 1
  • David A. Hart
    • 1
  • J. Wayne Streilein
    • 1
  1. 1.Departments of Internal Medicine, Microbiology, and Cell BiologyUniversity of Texas Health Science Center at DallasDallasUSA

Personalised recommendations