They found that patients who received mepolizumab were able to reduce their prednisone dose by 90% of their maximum possible compared to 55% in the placebo arm (p<0.05). 2000; Korenaga infection and in the encystment of larvae in (Gurish infection model in the two eosinophil lineage ablation mice lines (dblGATA and PHIL). They found that eosinophil ablation had no effect on worm burden or on egg deposition, indicating Nicardipine that eosinophil ablation has no impact on traditional measures of disease in the infection model in mice. However, the authors concluded: eosinophils may have unexplored immunomodulatory contributions to this disease process (Swartz reported that in contrast to results obtained on a BALB/c background, eosinophil-deficient C57BL/6 dbl-GATA mice have reduced airway hyperresponsiveness, and cytokine production of IL-4, -5, and -13 in OVA-induced allergic airway inflammation. This was caused by reduced T cell recruitment into the lung, as these mouse lungs had reduced expression of CCL7/MCP-3, CC11/eotaxin-1, and CCL24/eotaxin-2. These studies indicate that on the C57BL/6 background, eosinophils are integral to the Nicardipine development of airway allergic responses by modulating chemokine and/or cytokine production in the lung, leading to T cell recruitment (Walsh proposed an alternative hypothesis implicating eosinophils in the regulation of pulmonary T cell responses. This was supported by OVA-sensitized/challenged mice devoid of eosinophils (the transgenic line PHIL) that have reduced airway levels of Th2 cytokines that correlated with a reduced ability to recruit effector T cells to the lung. PALLD Indeed, they have shown that adoptive transfer of Th2-polarized OVA-specific transgenic T cells (OT-II) alone into OVA-challenged PHIL recipient mice failed to restore Th2 cytokines, airway histopathologies, and, the recruitment of pulmonary effector T cells (Jacobsen have shown that mice deficient in CCR3, mice deficient in both eotaxin-1 and eotaxin-2 and dbl-GATA have eosinophilic infiltration abolished by 94%, 98%, and 99% respectively. Importantly, Th2 lymphocyte cytokine production was impaired in the lungs of eosinophil- and CCR3-deficient mice as well as in allergen-induced mucus production (Fulkerson have shown abundant MBP positive staining in the skin of AD patients even in the absence of eosinophils (Davis induces AD-like skin inflammation but eosinophils do not migrate into the esophagus despite a strong systemic Th2 response, chronic cutaneous antigen exposure, accelerated bone marrow eosinophilopoiesis and circulating eosinophilia. However, when epicutaneously sensitized mice are subsequently exposed only once to intranasal antigen, esophageal eosinophilia (and lung inflammation) is powerfully induced (Akei studied, in a randomized Nicardipine placebo-controlled trial, the prednisone-sparing effect of mepolizumab on eosinophilic bronchitis with or without asthma. They found that patients who received mepolizumab were able to reduce their prednisone dose by 90% of their maximum possible compared to 55% in the placebo arm (p<0.05). Mepolizumab treatment was accompanied by a significant decrease in sputum and blood eosinophils and improvements in asthma control, FEV1 and asthma quality of life that were maintained for 8 weeks after the last infusion, suggesting that mepolizumab is an effective prednisone-sparing therapy in patients with eosinophilic bronchitis with or without asthma (Nair et al., 2008) Acknowledgments The Authors wish to thank the whole eosinophil field that built the concepts presented. Andrea lippelman, Katherine Henderson and LaWanda Bryant for administrative assistance. This work was supported by in part by the Thrasher Research Fund NR-0014 (C.B.), the PHS Grant P30 DK0789392 (C.B.), the NIH AI079874-01 (C.B.) AI070235, AI45898, and DK076893 (M.E.R.), the Food Allergy and Anaphylaxis Network (M.E.R.), Campaign Urging Research for Eosinophil Disorders (CURED), the Buckeye Foundation (M.E.R.) and The Food Allergy Project (M.E.R)..