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Άρθρα ανασκόπησης: Ανοσοθεραπεία, Δεκέμβριος 2013

Στο τεύχος του Δεκεμβρίου 2013 της περιοδικής έκδοσης Allergology  International δημοσιεύονται τρείς ανασκοπήσεις με κεντρικό θέμα τις πρόσφατες εξελίξεις στην ανοσοθεραπεία και τους μηχανισμούς της ανοσολογικής ανοχής.

Σε αντίστοιχα άρθρα, οι ομάδες των S. Durham και C. Akdis ανασκοπούν τα σύγχρονα δεδομένα σχετικά με την κατανόηση των ανοσολογικών μηχανισμών που διέπουν την ανοσοθεραπεία, την αποτελεσματικότητά της στην τροποποίηση της φυσικής πορείας των αλλεργικών νοσημάτων και επιπλέον τις νεωτερικές προσεγγίσεις για την δημιουργία αποτελεσματικότερων και ασφαλέστερων εμβολίων ανοσοθεραπείας, ενώ η ομάδα του G. Canonica αναφέρεται στον αναδυόμενο ρόλο της υπογλώσσιας ανοσοθεραπείας και συζητά τις μελλοντικές προοπτικές της.

Matsuoka T, Shamji MH, Durham SR.

Allergen immunotherapy and tolerance.

Allergol Int. 2013 Dec;62(4):403-13.

Abstract

Successful allergen-specific immunotherapy (AIT) is associated with a marked decrease in symptoms on allergen exposure, a reduced requirement for ‘rescue’ anti-allergic drugs and improvement in patients’ quality of life. These benefits persist for at least several years following discontinuation of immunotherapy – the hallmark of clinical and immunological tolerance. AIT has been shown to modulate both innate and adaptive immunological responses. Early suppression of innate effector cells of allergic inflammation (mast cells, basophils), regulation of pro-allergic T helper 2 type (Th 2) responses and IgE+ B cell responses have been shown to occur both in the tissue and in the peripheral blood during AIT. The allergen-tolerant state is associated with local and systemic induction of distinct populations of allergen-specific T regulatory cells including IL-10+ Tregs (Tr1 cells), TGF-β+ Tregs and FoxP3+ memory T regs. B cells are switched in favour of producing IgG (particularly IgG4) antibodies and associated blocking activity for IgE-dependent events, including basophil activation and IgE-facilitated allergen binding to B cells. An induction of IL-10+ B regulatory cells and alterations in dendritic cell subsets have also recently been described. These events are followed by the induction of T regulatory cells, suppression of allergen-specific T cell proliferation and immune deviation from Th2 in favour of Th1 responses. Alternative mechanisms of tolerance include apoptosis/deletion of antigen-specific memory Th2 cells and/or a failure of co-stimulation leading to T cell anergy.

Η πρόσβαση στο άρθρο είναι ελεύθερη από την ιστοσελίδα του εκδότη:

http://ai.jsaweb.jp/fulltext/062040403/062040403_index.html

 

Compalati E, Braido F, Walter Canonica G.

Sublingual immunotherapy: recent advances.

Allergol Int. 2013 Dec;62(4):415-23.

Abstract

The practice of administering sublingual immunotherapy for respiratory allergy is gaining more and more diffusion worldwide as a consequence of the robust demonstration of clinical efficacy and safety provided by recent high-powered and well-designed studies, confirming for individual seasonal allergens the results of previous metanalyses in adult and pediatric populations. Preliminary evidence derives from recent rigorous trials on perennial allergens, like house dust mites, and specifically designed studies addressed the benefits on asthma. Emerging research suggests that SLIT may have a future role in other allergic conditions such as atopic dermatitis, food, latex and venom allergy. Efforts to develop a safer and more effective SLIT for inhalant allergens have led to the development of allergoids, recombinant allergens and formulations with adjuvants and substances targeting antigens to dendritic cells that possess a crucial role in initiating immune responses. The high degree of variation in the evaluation of clinical effects and immunological changes requires further studies to identify the candidate patients to SLIT and biomarkers of short and long term efficacy. Appropriate management strategies are urgently needed to overcome the barriers to SLIT compliance.

Η πρόσβαση στο άρθρο είναι ελεύθερη από την ιστοσελίδα του εκδότη:

http://ai.jsaweb.jp/fulltext/062040415/062040415_index.html

 

Jutel M, Van de Veen W, Agache I, Azkur KA, Akdis M, Akdis CA.

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

Allergol Int. 2013 Dec;62(4):425-33.

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.

Η πρόσβαση στο άρθρο είναι ελεύθερη από την ιστοσελίδα του εκδότη:

http://ai.jsaweb.jp/fulltext/062040425/062040425_index.html

 

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