Allergic airway response

Lambert, A.L., et al., Transfer of allergic airway responses with serum and lymphocytes from rats sensitized to dust mite, Am. J. Respir. Crit. Care Med., 157, 1991, 1998. 

Talati, M., Meyrick, B., Peebles, R.S., Jr., Davies, S.S., Dworski, R., Mernaugh, R., Mitchell, D., Boothby, M., Roberts, L.J., and Sheller, J.R. Oxidant stress modulates murine allergic airway responses. Free Radic Biol Med 40 (2006) 1210-1219. 

Lukacs, N. W., Tekkanat, K. K., Berlin, A., Hogaboam, C. M., Miller, A., Evanoff, H., Lincoln, P., and Maassab, H. (2001). Respiratory syncytial virus predisposes mice to augmented allergic airway responses via IL-13-mediated mechanisms. J. Immunol. 167, 1060. 

Schuh, J., Blease, K., Kunkel, S., and Hogaboam, C. (2002). Eotaxin/CCL 11 is involved in acute, but not chronic, allergic airway responses to Aspergillus fumigatus. Am. J. Physiol. Lung. Cell. Mol. Physiol. 283, L198-L204. 

Sedgwick JB, Calhoun WJ, Gleich GJ, Kita H, Abrams JS, Schwartz LB, Volovitz B, Ben-Yaakov M, Busse WW. Immediate and late allergic airway response to segmental antigen. Characterization of eosinophil and mast cell mediators. Am Rev Respir Dis 1991 144 1274-1281. 

Goya I, Villares R, Zaballos A, et al. Absence of CCR8 does not impair the response to ovalbumin-induced allergic airway disease. J Immunol 2003 170(4) 2138-2146. 

John AE, Gerard CJ, Schaller M, et al. Respiratory syncytial virus-induced exaggeration of allergic airway disease is dependent upon CCRI-associated immune responses. Eur J Immunol 2005 35(1) 108-116. 

Mast Cells Initiate and ModulateT-Cell Responses during Allergic Airway Inflammation... 

Winkler B, Baier B, Wagner S, Repa A, Scheiner O, Kraft D, Wiedermann U Mucosal tolerance as therapy of type I allergy Intranasal application of recombinant Bet v 1, the major birch pollen allergen, leads to the suppression of allergic immune responses and airway inflammation in sensitized mice. Clin Exp Allergy 2002 32 30-36. 

Th2 cytokine IL-10 is an antiinflammatory cytokine that suppresses the secretion of proinflammatory cytokines (Dll), allergen-induced airway inflammation, and nonspecific airway responsiveness (T9). IL-13 shares a receptor component, signaling pathways, and many biological activities with IL-4. In fact, IL-13 is also an antiinflammatory cytokine and plays a unique role in the optimal induction and maintenance of IgE production and IgE-mediated allergic responses when IL-4 production is low or absent (DIO, W12). Moreover, IL-13 or IL-4 shows a synergistic effect with TNF-a or IL-5 on eosinophil activation (L20). Recently, IL-11 was found to be involved in the chronic remodeling seen in asthmatic airways and is associated with increasing severity of the disease (Ml6). 

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