A regulatory role for the C5a anaphylatoxin in type 2 immunity in asthma
J. Clin. Invest. Jörg Köhl, et al. 116:783 doi:10.1172/JCI26582 [Go to this article.]

Figure 1
Protocols underlying the different models of pulmonary allergy. (A) OVA model of inhalation tolerance. Animals were exposed to i.t. OVA at the indicated time points. To block C5aR signaling, animals were treated with anti-C5aR mAb on days –1 and 20. Twenty-four hours after the final allergen exposure, airway responsiveness was determined. Subsequently, BAL, lung tissue, and blood samples were taken. (B) HDM model of pulmonary allergy in which the C5aR was blocked during initial allergen exposure. Animals were exposed to i.t. HDM at the indicated time points (left panel). To block C5aR signaling, animals were treated with the anti-C5aR mAb on days –1, 6, 13, and 20. Seventy-two hours after the final HDM exposure, airway responsiveness was determined. Subsequently BAL, lung tissue, and blood samples were taken. For right panel, procedure was as above, except that the C5aR was blocked by pulmonary expression of the C5aRA. C5aRA expression was initiated 7 days prior to allergen exposure by supplementing the drinking water with dox (0.5 mg/ml). Dox was kept in the drinking water throughout the experiment. (C) Procedure was as in B, except that the C5aR was blocked solely prior to the final HDM exposure on day 20.