Sensitization and tolerance

Curr Opin Allergy Clin Immunol. 2001 Jun;1(3):237-41. doi: 10.1097/01.all.0000011020.20431.84.

Abstract

The mechanisms responsible for sensitization, in particular within the gastrointestinal tract, are IgE-mediated as well as of a non-IgE-mediated, immunological origin. The phenomenon that is the opposite of sensitization is the maintenance of tolerance and is exemplified by the phenomenon 'oral tolerance'. The cytokines transforming growth factor beta and interferon gamma have been shown to be key immunoregulatory cytokines in oral tolerance. A new experimental model of eosinophilic allergic gastroenteritis has been developed with the use of encapsulated dietary antigen. The model was used in mice with genetic deletions of the eosinophil chemokine eotaxin or of the cytokine IL-5, demonstrating the importance of eotaxin. In clinical allergy research, a major question has been to explain the global increase in asthma and allergy. The 'hygiene hypothesis' states that a lack of maturation of the infant immune system from a T helper 2 to a T helper 1 type of immune response may be caused by less microbial stimulation in Western societies. Several lines of data support this hypothesis. However, apart from the genetic constitution of the individual, breastfeeding in infancy may be the most important single determinant for the development of clinical tolerance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bacterial Infections / immunology
  • Breast Feeding
  • Chemokines / physiology
  • Disease Models, Animal
  • Humans
  • Hypersensitivity / etiology*
  • Immune Tolerance*
  • Infant, Newborn
  • Lipopolysaccharide Receptors
  • Risk Factors
  • T-Lymphocytes / immunology

Substances

  • Chemokines
  • Lipopolysaccharide Receptors