Mechanisms of allergen-specific immunotherapy and novel ways for vaccine development

Allergol Int. 2013 Dec;62(4):425-33. doi: 10.2332/allergolint.13-RAI-0608. Epub 2013 Oct 25.

Abstract

Allergen-specific immunotherapy (SIT) is the only available curative treatment of allergic diseases. Recent evidence provided a plausible explanation to its multiple mechanisms inducing both rapid desensitization and long-term allergen-specific immune tolerance, and suppression of allergic inflammation in the affected tissues. During SIT, peripheral tolerance is induced by the generation of allergen-specific regulatory T cells, which suppress proliferative and cytokine responses against the allergen of interest. Regulatory T cells are characterized by IL-10 and TGF-beta secretion and expression of important cell surface suppressive molecules such as cytotoxic T lymphocyte antigen-4 and programmed death-1 that directly or indirectly influence effector cells of allergic inflammation, such as mast cells, basophils and eosinophils. Regulatory T cells and particularly IL-10 also have an influence on B cells, suppressing IgE production and inducing the production of blocking type IgG4 antibodies. In addition, development of allergen-specific B regulatory cells that produce IL-10 and develop into IgG4 producing plasma cells represent essential players in peripheral tolerance. These findings together with the new biotechnological approaches create a platform for development of the advanced vaccines. Moreover, reliable biomarkers could be selected and validated with the intention to select the patients who will benefit most from this immune-modifying treatment. Thus, allergen-SIT could provide a complete cure for a larger number of allergic patients and novel preventive approaches need to be elaborated.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Allergens / immunology
  • B-Lymphocytes, Regulatory / immunology*
  • Basophils / immunology
  • CTLA-4 Antigen / metabolism
  • Desensitization, Immunologic / methods*
  • Desensitization, Immunologic / trends
  • Eosinophils / immunology
  • Humans
  • Hypersensitivity / immunology
  • Hypersensitivity / therapy*
  • Immune Tolerance
  • Immunoglobulin E / metabolism
  • Interleukin-10 / immunology
  • Mast Cells / immunology*
  • Programmed Cell Death 1 Receptor / metabolism
  • T-Lymphocytes, Regulatory / immunology*
  • Transforming Growth Factor beta / immunology
  • Vaccines / immunology*

Substances

  • Allergens
  • CTLA-4 Antigen
  • CTLA4 protein, human
  • Programmed Cell Death 1 Receptor
  • Transforming Growth Factor beta
  • Vaccines
  • Interleukin-10
  • Immunoglobulin E