Research over the past decade has provided information concerning the onset and treatment of allergic diseases, including bronchial asthma, allergic rhinitis and atopic dermatitis. Recent studies also indicated that allergic inflammation is the basic pathophysiology of allergic diseases and is closely associated with their progression and exacerbation. Our understanding of the mechanism of allergic inflammation with regard to therapeutic agents has improved as a result of immunological and molecular biological studies.

While much effort has been paid to developing a new anti-allergic drug, allergic disease has yet to be completely conquered. More extensive research will allow the development of new therapeutics to combat allergic diseases. This article provides an overview of recent advances in the development of anti-allergic drugs．

The increasing incidence in allergic diseases, including allergic bronchial asthma, allergic rhinoconjunctivitis and atopic dermatitis, is as yet unexplained. Pathomechanistic studies have indicated that allergic inflammation contributes to onset of acute andor chronic symptoms of allergic diseases. Despite our understanding of the underlying mechanism, there are some therapeutic problems because the prevalence of allergic diseases has increased dramatically in recent decades . A significant amount of research is currently focused on explaining this rise in the number of cases of allergic diseases.

Future drugs

Future strategy aimed at down regulation of the allergic response can be classified into many categories as indicated. While there are numerous possible strategies to develop a new drug, our interest is focused on the concept of Th2 dependent allergic inflammation in the diseases. With regard to the suppression of Th2 response, there are some new trials targeting Th 1 response stimulation, cytokine suppression and other regulatory molecules. One of the Th1 stimulators is a plasmid vector containing genes that encode allergen, namely a DNA vaccine.51,52

This vaccine decreases Th2-mediated responses, enhances Th1 mediated responses and suppresses allergic responses in animal models. Other trials have employed a virus-like particle to induce interferon producing CD8+T cells and mucosal DNA vaccines to induce tolerance.53 For example, the main peanut allergen gene expression vector when administered orally caused higher fecal IgA and serum IgG2a and lowered serum IgE titer and resulted in decreased anaphylactic symptoms . 54 Whether this approach is efficacious will be determined in further studies．

A particular approach for enhancement of Th1 mediated response has been the administration of synthetic oligodeoxynucleotides with immunostimulatory sequences. Strong stimulation was driven by sequences containing methylated CpG motifs that are more highly expressed in microbial rather than vertebrate DNA, and so are recognized as foreign by the Toll-like receptor in innate immunity. These motifs indicate the function as Th1 promoting adjuvant capable of switching the usual Th2 response toward Th1 response.

Preclinical results are promising, but the outcome of clinical trials for allergic diseases is pending． Some experimental results, including those of our own, indicate the efficacy of interferons or IL-12 against allergic inflammation.

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Regards

Mary Wilson

Editorial office

Clinical Pharmacology and Toxicology Research

E-mail: pharmatoxicol@eclinicalsci.com