Of importance, treatment with anti-IL-17 antibodies has been shown to ameliorate clinical symptoms of psoriasis, and arthritis in clinical trials. Therefore, targeting Th17 cytokines may provide a promising therapeutic approach for the treatment of numerous chronic inflammatory human diseases. Increased levels of IL-17 were detected in the lung, sputum and bronchoalveolar lavage fluids of asthmatic patients, suggesting a possible involvement of Th17 cells in asthma. While Th2 responses promote eosinophilic inflammation in the lungs, Th17 responses have been suggested to play a non-redundant role in pulmonary inflammation by inducing neutrophilic inflammation. Elevated neutrophilia is correlated to asthma severity. Supporting this notion, recent studies have shown that the IL-17 from pulmonary T cells enhances airway hyper-responsiveness and neutrophilic inflammation in animal models of asthma. On the other hand, it has been shown that neutralizing IL-17 augments allergic responses in the lung, and that administration of IL-17 ameliorates eosinophilia and airway hypersensitivity in an animal model of asthma, suggesting that IL-17 suppresses lung inflammation. In addition, the negative regulation of allergic 
lung inflammation by IL-17-producing cd T cell has been described. Thus, the biological roles of Th17 responses in allergic lung diseases are presently not well defined, and the overall impact of Th17 cells in allergic asthma remains controversial. The cellular and molecular mechanisms mediated by Th17 cells during allergic asthma are likely complex; therefore, extensive further investigation will be required before the overall picture of how Th17 cells influence the allergic response to lung allergens can be fully visualized. The complement system is primarily known for its crucial host defense against bacterial and viral infections through opsonization and formation of the membrane attack complex. Activation of complement by invading pathogens generates various cleavage products including the anaphylatoxins C5a and C3a. C3a mediates diverse functions in the immune system upon binding to its receptor C3aR, which is expressed on certain parenchymal cells, such as lung epithelial cells, and on numerous myeloid cells including neutrophils, macrophages, mast cells and basophils. Lomitapide Mesylate patients with asthma exhibit elevated levels of C3a in the sera as well as in the airway. C3aR-deficient mice exhibit a decreased number of eosinophils in the airway with reduced Th2 responses and less airway hyperresponsiveness in experimental asthma models. In addition, administration of C3aR 3,4,5-Trimethoxyphenylacetic acid antagonist ameliorates the airway inflammation induced by allergens in mice. Although these previous studies have made a strong case for C3a as a pathogenic mediator of allergic lung disease, only recently has the impact of C3a on IL-17 in the context of allergic asthma been investigated. For instance, it has been recently shown that C3aR2/2 mice produce less IL-17 when challenged with house dust mite allergens than wild-type challenged mice. In the same study, it was demonstrated that C3a promotes IL-17 production upon allergenic challenge in the lung by suppressing IL-10 production while inducing IL-23 from dendritic cells. However, in the inflamed lung, IL-17 can be generated by CD4 + T cells as well as innate immune cells including cd T cells, NKT cells, and alveolar macrophages. Since the C3aR has been reported to be expressed on macrophages and other bone marrow derived cells, the C3a-dependent IL-17 phenotype observed in this dust mite mouse model may be due to more extensive cellular.