WO 2005/118615 PCT/US2005/019594 INHIBITORS OF REGIII PROTEINS AS ASTHMA THERAPEUTICS FIELD OF THE INVENTION [0001] It is an object of the invention to provide methods of screening for agents for treating asthma. It is a further object of the invention to provide methods for treating asthma. These and other objects and advantages of the present invention will be apparent from the descriptions herein. BACKGROUND OF THE INVENTION [0002] The present invention relates generally to asthma therapeutics. Specifically, the invention relates to methods of screening for agents for treating asthma and methods for treating asthma. [0003] Asthma is a chronic inflammatory disease of the airways characterized by recurrent episodes of reversible airway obstruction and airway hyperresponsiveness (AHR). Typical clinical manifestations include shortness of breath, wheezing, coughing and chest tightness that can become life threatening or fatal. While existing therapies focus on reducing the symptomatic bronchospasm and pulmonary inflammation, there is a growing awareness of the role of long term airway remodeling in accelerated lung deterioration in asthmatics. Airway remodeling refers to a number of pathological features including epithelial smooth muscle and myofibroblast hyperplasia and/or metaplasia, subepithelial fibrosis and matrix deposition. The processes collectively result in up to about 300% thickening of the airway in cases of fatal asthma. Despite the considerable progress that has been made in elucidating the pathophysiology of asthma, the prevalence, morbidity, and mortality of the disease has increased during the past two decades. In 2000, in the United States alone, nearly 1.8 million emergency room visits, 465,000 hospitalizations and 4,487 deaths were directly attributed to asthma. Asthma-related healthcare costs are estimated at $14 billion annually. [0004] It is generally accepted that allergic asthma is initiated by an inappropriate inflammatory reaction to airborne allergens. The lungs of asthmatics demonstrate an intense infiltration of lymphocytes, mast cells and especially eosinophils. A large WO 2005/118615 PCT/US2005/019594 body of evidence has demonstrated this immune response is driven by CD4+ T-cells expressing a TH2 cytokine profile. One murine model of asthma involves sensitizatio: of the animal to ovalbumin (OVA) followed by intratracheal delivery of the OVA challenge. This procedure generates a TH2 immune reaction in the mouse lung and mimics four major pathophysiological responses seen in human asthma, including upregulated serum IgE (atopy), eosinophilia, excessive mucus secretion, and AHR. The cytokine IL-13, expressed by basophils, mast cells, activated T cells and NK cells plays a central role in the inflammatory response to OVA in mouse lungs. Direct lun£ instillation of murine IL-13 elicits all four of the asthma-related pathologies and, conversely, the presence of a soluble IL-13 antagonist (sIL-13Ra2-Fc) completely blocked both the OVA-challenge induced goblet cell mucus synthesis and the AHR to acetylcholine. Wills-Karp, M.,et al., "Interleukin-13: central mediator of allergic asthma," Science 282(5397): 2258-2261 (1998); Grunig, G., et al, "Requirement for IL-13 independently of IL-4 in experimental asthma," Science 282(5397): 2261-2263 (1998). Thus, IL-13 mediated signaling is sufficient to elicit all four asthma-related pathophysiological phenotypes and is required for the hypersecretion of mucus and induced AHR in the mouse model. [0005] Biologically active IL-13 binds specifically to a low-affinity binding chain IL-13Rotl and to a high-affinity multimeric complex composed of IL-13Ral and IL-4R, a shared component of IL-4 signaling complex. Wills-Karp, M., "IL-12/IL-13 axis in allergic asthma," JAllergy Clin Immunol 107(1): 9-18 (2001). Activation of the IL-13 pathway cascade triggers the recruitment, phosphorylation and ultimate nuclear translocation of the transcription al activator Stat6. A number of physiological studies demonstrate the inability of pulmonary OVA-challenge to elicit major pathology related phenotypes including eosinophil infiltration, mucus hypersecretion and airway hyperreactivity in mice homozygous for the Stat6"'" null allele. Kuperman, D., et al, "Signal transducer and activator of transcription factor 6 (Stat6)- deficient mice are protected from antigen-induced airway hyperresponsiveness and mucus production," J Exp Med 187(6): 939-48 (1998). Recent genetic studies have demonstrated a linkage between specific human alleles of IL-13 and its signaling components with asthma and atopy, demonstrating the critical role of this pathway in -2- WO 2005/118615 PCT/US2005/019594 the human disease. Shirakawa et al., "Atopy and asthma: genetic variants of IL-4 and IL-13 signaling," Immunol. Today 21(2):60-64 (2000). [0006] IL-13 also binds to an additional receptor chain, IL-13Ra2, expressed in both human and mouse with as yet undefined biological function. The murine 3L-13R