IMMUNOLOGY - Roit A. - Mir 2000

Chapter 23. Hypersensitivity - Type I

THE BENEFICIAL ROLE OF IgE

Given that such numerous adverse effects are associated with the IgE response, the question arises as to why Antibodies of this Class ever evolved in the first place.

It has long been believed that IgE plays a primary role in defense against helminths; the mechanisms of this effect are illustrated in Fig. 18.9. Helminths parasitizing the intestine secrete soluble allergens that provoke an exceptionally strong IgE, as well as IgG, response in the gut-associated lymphoid tissue (GALT). Mast Cells maturing in the GALT are sensitized by IgE and migrate into the intestinal mucosa, where, upon contact with helminth Antigens, these cells undergo degranulation, releasing mediators that increase vascular permeability and recruit inflammatory cells, particularly eosinophils, to the area. IgE from the Lymph Nodes also sensitizes the helminths themselves to the action of eosinophils, which possess Fc receptors for IgE. As a result of the mediator-induced increase in vascular permeability—caused by substances such as histamine—Complement and helminth antigen-specific IgG also enter the inflammatory site. Simultaneously, mucus production by mucosal goblet cells increases. All of these factors lead to the damage and expulsion of the helminths from the body.

Since approximately one-third of the global human population is infected with helminths, it is quite possible that the IgE class arose as a result of selective pressure, with allergy thereby turning out to be an undesirable evolutionary side effect.

Questions for Structure/133.html">Discussion

■ Are Th2 cells (and the cytokines they produce) the single most important factors in the Pathogenesis of allergy? Is this statement correct?

■ If you were engaged in developing new therapeutic approaches for treating allergies, which path would you follow?

■ What measures should be taken for the specific blockade of late-phase reactions in the Lungs, and will this affect the asthmatic response?

■ How can the relative roles of genetic and environmental factors in The Development of allergy be investigated?

■ What accounts for the spread of allergic diseases among the population—from 1–2% in the 1900s to nearly 30% at present?

■ Is allergic asthma truly an example of delayed-type hypersensitivity in the lungs?

Introduction/47.html">Further Reading

Beaven M.A., Metzger H. 1993. Signal Transduction by Fc receptors: The FcεRI case. Immunol. Today 14: 222-6.

Bruynzeel-Koomen C., Wichen D., Toonstra J. et al. 1986. The presence of IgE molecules on epidermal Langerhans’ cells in patients with atopic dermatitis. Arch. Dermatol. Res. 278: 199-205.

Coca A.F., Cooke R.A. 1923. On the Classification of the phenomenon of hypersensitiveness. J. Immunol. 8: 163.

Cooke R.A., Vander-Veer A. 1916. Human sensitization. J. Immunol. 1: 201.

de Vries J.E. 1994. Novel fundamental approaches to intervening in IgE-mediated allergic diseases. J. Invest. Dermatol. 102: 141-4.

Galli S.J. 1993. New concepts about the mast Cell. N. Engl. J. Med. 328: 257-65.

Geha R.F. 1992. Regulation of IgE synthesis in humans. J. Allergy Clin. Immunol. 90: 143-50.

Gordon J. 1991. CD23: a novel disease marker with a split personality. Clin. Exp. Immunol. 86: 356-9.

Gordon J.R., Burd P.R., Galli S.J. 1990. Mast cells as a source of multifunctional cytokines. Immunol. Today 11: 458-64.

Juto P. 1980. Elevated serum immunoglobulin E in T cell deficient infants fed cow’s milk. J. Allergy Clin. Immunol. 66: 402.

Kaliner M.A. 1987. The late-phase reaction and its clinical implications. Hosp. Pract. 15(Oct): 73-83.

Kharitonov S.A., Yates D., Robbins R.A. et al. 1994. Increased nitric oxide in exhaled air of asthmatic patients. Lancet 343: 133-5.

Marsh D.G.. Neely J.D., Breazeale D.R. et al. 1994. Linkage analysis of IL-4 and other chromosome 5q31.1 markers and total serum immunoglobulin E concentrations. Science 264: 1152-6.

Miller J.S., Schwartz L.B. 1989. Human mast cell proteases and mast cell heterogeneity. Curr. Opin. Immunol. 1: 637-42.

Montfort S., Robinson H.C., Holgate S.T. 1992. The bronchial epithelium as a target for inflammatory attack in asthma. Clin. Exp. Immunol. 22: 511-20.

O'Hehir R.E., Lamb J.R. 1992. Strategies for modulating immunoglobulin E synthesis. Clin. Exp. Allergy 22: 7-10.

Prausnitz C., Kustner H. In. Gell PGH, Coombes RRA (eds). 1962. Clinical Aspects of Immunology. Oxford: Blackwel Scientific Publications. 808-16 (Appendix).

Romagnam S. 1992. Human Th1 and Тн2 subsets: Regulation of differentiation and role in protection and immunopathology. Int. Arch. Allergy Immunol. 98: 279-85.

Sedgwick J.D., Holt P.G. 1986. Induction of IgE- secreting cells in the lymphatic drainage of the lungs of rats following passive antigen inhalation. Int. Arch. Allergy Appl. Immunol. 79: 329-31.

Shau-Ku H., Marsh D.G. 1993. Genetics of allergy. Ann. Allergy 70: 347-58.

Spry C.J.F., Jay A.B., Gleich G.J. 1992. Eosinophils. Immunol. Today 13: 384-7.

Sutton B.J., Gould H.J. 1993. The human IgE network. Nature 366: 421-8.

Takafuji S., Suzukki S.. Koizumi K., et al. 1987. Diesel- exhaust particulates inoculated by the intranasal route have adjuvant activity for IgE production in mice. J. Allergy Clin. Immunol. 79: 639-45.

Wide L., Bennich H., Johansson S.G.O. 1967. Diagnosis of allergy by an in vitro test for allergen antibodies. Lancet ii: 1105.



Last update: 13/08/2026

Editorial and Educational Adaptation: This material has been compiled based on the primary/original source text. The project team performed an editorial review, corrected technical inaccuracies, structured sections, and adapted the content for an educational format.

What was processed:

  • elimination of formatting defects (OCR errors, structural breaks, corrupted characters);
  • editorial organization of content;
  • standardization of terminology in accordance with academic sources;
  • verification of factual statements against the original source text.

All mentions of the author, publication year, and origin of the primary text have been preserved in accordance with the source.