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CpG Oligodeoxynucleotides in Asthma

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Microbial DNA and Host Immunity
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Abstract

Asthma is recognized as chronic airway inflammation characterized by airway eosinophilic inflammation and airway hyperreactivity (1). It is also highly correlated with atopy, and antigen-induced immunoglobulin E (IgE) production is increased in patients with allergic asthma (2). Interleukin-5 (IL-5) is the terminal differentiation, activation, and survival factor for eosinophils (3,4). IL-4 amplifies the asthmatic inflammatory response through IgE class switching (5) and stimulating growth of mast cells (6). IL-13 also plays a role in IgE synthesis (7). CD4-positive T lymphocytes can be divided in to type 1 helper T (Th1) and type 2 helper T (Th2) cells on the basis of their cytokine production pattern (8). Th2 cells can produce IL-4, IL-5, and IL-13. Therefore, although mast cells and eosinophils also can secrete these cytokines (9,10), Th2 cells are seen as having a central role for pathogenesis of asthma since they produce these proinflammatory mediators in antigenspecific responses (11). Th 1 cells produce IL-2 and interferon γ (IFN-γ) and none of the Th2 cytokines. Th1 and Th2 cells are counter-regulatory through their cytokine production. For example, IL-4 promotes Th2 development (12) and inhibits Th 1 cells (13). In contrast, IFN-y promotes Th1 development (12) and inhibits the proliferation of Th2 cells (14) and the synthesis of IL-4 and IL-5 by Th2 cells (15). Th1 and Th2 cells have been identified in humans (16–18). These lines of evidences suggest that inhibition of Th2 cytokine production or enhancement of Th1 cytokine production may be useful in the treatment of asthma.

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Kitagaki, K., Kline, J.N. (2002). CpG Oligodeoxynucleotides in Asthma. In: Raz, E. (eds) Microbial DNA and Host Immunity. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-305-7_24

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