Mast Cells: Immunologically Specific Effectors and Potential Sources of Multiple Cytokines During IgE-Dependent Responses

  1. Derek J. Chadwick Organizer,
  2. David Evered Organizer and
  3. Julie Whelan
  1. Stephen J. Galli1,
  2. Barry K. Wershil1,2,
  3. John R. Gordon1 and
  4. Thomas R. Martin1,3

Published Online: 28 SEP 2007

DOI: 10.1002/9780470513866.ch5

Ciba Foundation Symposium 147 - IgE, Mast Cells and the Allergic Response

Ciba Foundation Symposium 147 - IgE, Mast Cells and the Allergic Response

How to Cite

Galli, S. J., Wershil, B. K., Gordon, J. R. and Martin, T. R. (2007) Mast Cells: Immunologically Specific Effectors and Potential Sources of Multiple Cytokines During IgE-Dependent Responses, in Ciba Foundation Symposium 147 - IgE, Mast Cells and the Allergic Response (eds D. J. Chadwick, D. Evered and J. Whelan), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470513866.ch5

Author Information

  1. 1

    Departments of Pathology, Beth Israel Hospital and Harvard Medical School, and the Charles A. Dana Research Institute, Beth Israel Hospital, 330 Brookline Avenue, Boston, MA 02215, USA

  2. 2

    Combined Pediatric Gastroenterology and Nutrition Program, Harvard Medical School, Boston, MA 02115, USA

  3. 3

    Department of Pediatrics, Children's Hospital, (Ina Sue Perlmutter Laboratory), Boston, MA 02115, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471923091

Online ISBN: 9780470513866

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Keywords:

  • mast cells;
  • cytokines;
  • IgE-dependent responses;
  • microenvironmental regulation;
  • mast cell phenotype

Summary

Mast cells are critical effectors in many IgE-dependent responses, and the numbers and phenotype of certain mast cell populations can be influenced, through IL-3 and IL-4, by the same T cells that regulate IgE production. However, IgE can interact with cells other than mast cells, and different mast cell populations express significant variation in multiple important aspects of their phenotype, including mediator content and responses to cytokines and stimuli of activation. As a result it may be difficult to define the unique contributions of mast cells to IgE-dependent reactions. One approach for analysing the roles of various mast cell populations in individual biological responses is to attempt to elicit these reactions in mice in which the presence or absence of specific mast cell populations can be regulated experimentally. We have used genetically mast cell-deficient and mast cell-reconstituted mice to demonstrate that mast cells provide essential effector function in certain IgE-dependent responses involving the skin, stomach or lungs but are not necessary for the pulmonary alterations and death associated with active anaphylaxis. Similar approaches can be used to investigate the biological significance of the production, by mast cells stimulated with IgE and specific antigen, of cytokines similar or identical to IL-I, IL-3, IL-4, 1L-5, IL-6, TNF-αcachectin, IFN-γ, GM-CSF, JE, MIP-1β, MIP-IP and TCA3.