| Title | Basophil-derived interleukin-4 controls the function of natural helper cells, a member of ILC2s, in lung inflammation. |
| Publication Type | Journal Article |
| Year of Publication | 2014 |
| Authors | Motomura, Y, Morita, H, Moro, K, Nakae, S, Artis, D, Endo, TA, Kuroki, Y, Ohara, O, Koyasu, S, Kubo, M |
| Journal | Immunity |
| Volume | 40 |
| Issue | 5 |
| Pagination | 758-71 |
| Date Published | 2014 May 15 |
| ISSN | 1097-4180 |
| Keywords | Animals, Asthma, Basophils, Chemokine CCL11, Eosinophils, Interleukin-13, Interleukin-4, Interleukin-5, Interleukin-9, Mice, Mice, Inbred C57BL, Mice, Knockout, Pneumonia, Pulmonary Eosinophilia, T-Lymphocytes, Helper-Inducer |
| Abstract | <p>Allergic asthma is an inflammatory disease characterized by lung eosinophilia controlled by type 2 cytokines. Cysteine proteases are potent triggers of allergic inflammation by causing barrier disruption in lung epithelial cells inducing the elevation of interleukin-5 (IL-5) and IL-13 from natural helper (NH) cells, a member of ILC2s, which leads to lung eosinophilia. In this study, we found that basophils play a crucial role in NH cell-mediated eosinophilic inflammation induced by protease allergens. Conditional deletion of basophils caused a resolution of the papain-induced eosinophilia and mucus production. Resolution of eosinophilia was also observed in mice lacking IL-4 specifically in basophils, indicating that basophil-derived IL-4 enhanced expression of the chemokine CCL11, as well as IL-5, IL-9, and IL-13 in NH cells, thus attracting eosinophils. These results demonstrate that IL-4 from basophils has an important role in the NH-derived cytokine and chemokine expression, subsequently leading to protease allergen-induced airway inflammation.</p> |
| DOI | 10.1016/j.immuni.2014.04.013 |
| Alternate Journal | Immunity |
| PubMed ID | 24837103 |