Mechanisms of allergen-specific immunotherapy.

Allergen-specific immunotherapy (SIT) is the only treatment, which leads to a life-long tolerance against allergens due to restoration of normal immunity. The induction of a tolerant state in peripheral T cells represents an essential step in allergen-SIT. Peripheral T-cell tolerance is characterized mainly by suppressed proliferative and cytokine responses against the major allergens and its T-cell recognition sites. It is initiated by autocrine action of IL-10 and/or TGF-Beta, which are increasingly produced by the antigen-specific T Regulatory (T(Reg)) cells. Tolerized T cells can be reactivated to produce either of the distinct Th1 or Th2 cytokine patterns, thus directing allergen-SIT towards successful or unsuccessful treatment. T(Reg) cells directly or indirectly influence effector cells of allergic inflammation, such as mast cells, basophils and eosinophils. In addition, there is accumulating evidence that they may suppress IgE production and induce IgG4 and IgA production against allergens. By the application of the recent knowledge in mechanisms of allergen-SIT, more rational and safer approaches are awaiting in the future for the prevention and cure of allergic diseases.

[1]  C. Akdis,et al.  T cells and eosinophils cooperate in the induction of bronchial epithelial cell apoptosis in asthma. , 2002, The Journal of allergy and clinical immunology.

[2]  R. Aalberse,et al.  IgG4 breaking the rules , 2002, Immunology.

[3]  Min Zhang,et al.  A novel human immunoglobulin Fc gamma Fc epsilon bifunctional fusion protein inhibits Fc epsilon RI-mediated degranulation. , 2002, Nature medicine.

[4]  C. Akdis,et al.  Role of IL-10 in allergen-specific immunotherapy and normal response to allergens. , 2001, Microbes and infection.

[5]  A. Sewell,et al.  Bypassing IgE and targeting T cells for specific immunotherapy of allergy , 2001 .

[6]  I. Bellinghausen,et al.  Decreased release of histamine and sulfidoleukotrienes by human peripheral blood leukocytes after wasp venom immunotherapy is partially due to induction of IL-10 and IFN-gamma production of T cells. , 1999, The Journal of allergy and clinical immunology.

[7]  G. Canonica,et al.  Randomised controlled trial of local allergoid immunotherapy on allergic inflammation in mite-induced rhinoconjunctivitis , 1998, The Lancet.

[8]  W. Dolen,et al.  Use of thiocyanate elution to estimate relative avidity of allergen specific IgE antibodies. , 1997, Allergy and asthma proceedings.

[9]  P. Venge,et al.  Priming of eosinophil adhesion in patients with birch pollen allergy during pollen season: effect of immunotherapy. , 1997, The Journal of allergy and clinical immunology.

[10]  R. Ree,et al.  Measurement of IgE antibodies against purified grass pollen allergens (Lol p 1, 2, 3 and 5) during immunotherapy , 1997, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[11]  M. Jutel,et al.  Influence of bee venom immunotherapy on degranulation and leukotriene generation in human blood basophils , 1996, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[12]  C. Akdis,et al.  Epitope-specific T cell tolerance to phospholipase A2 in bee venom immunotherapy and recovery by IL-2 and IL-15 in vitro. , 1996, The Journal of clinical investigation.

[13]  M. Jordana,et al.  Interleukin (IL)-10 inhibits long-term IL-6 production but not preformed mediator release from rat peritoneal mast cells. , 1996, The Journal of clinical investigation.

[14]  B. Eberlein-König,et al.  Tryptase and histamine release due to a sting challenge in bee venom allergic patients treated successfully or unsuccessfully with hyposensitization * , 1995, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[15]  M. Goldman,et al.  B7/CD28-dependent IL-5 production by human resting T cells is inhibited by IL-10. , 1994, Journal of immunology.

[16]  P. Venge,et al.  Immunotherapy abrogates the generation of eosinophil and neutrophil chemotactic activity during pollen season. , 1990, The Journal of allergy and clinical immunology.

[17]  N. Yamaguchi,et al.  Transforming growth factor beta induces IgA production and acts additively with interleukin 5 for IgA production , 1989, The Journal of experimental medicine.

[18]  A. Helbling,et al.  Predictive value of venom‐specific IgE, IgG and IgG subclass antibodies in patients on immunotherapy with honey bee venom , 1989, Allergy.

[19]  J. Bousquet,et al.  Double-blind, placebo-controlled immunotherapy with mixed grass-pollen allergoids. II. Comparison between parameters assessing the efficacy of immunotherapy. , 1988, The Journal of allergy and clinical immunology.

[20]  P. Venge,et al.  The effect of immunotherapy on bronchial hyperresponsiveness and eosinophil cationic protein in pollen-allergic patients. , 1988, The Journal of allergy and clinical immunology.

[21]  R. Naclerio,et al.  Nasal challenge with ragweed pollen in hay fever patients. Effect of immunotherapy. , 1985, The Journal of clinical investigation.

[22]  G. Gleich,et al.  Effect of immunotherapy on immunoglobulin E and immunoglobulin G antibodies to ragweed antigens: a six-year prospective study. , 1982, The Journal of allergy and clinical immunology.

[23]  D. Meyers,et al.  Clinical relevance of the venom-specific immunoglobulin G antibody level during immunotherapy. , 1982, Journal of Allergy and Clinical Immunology.