| First Author | Willart MA | Year | 2012 |
| Journal | J Exp Med | Volume | 209 |
| Issue | 8 | Pages | 1505-17 |
| PubMed ID | 22802353 | Mgi Jnum | J:189157 |
| Mgi Id | MGI:5444555 | Doi | 10.1084/jem.20112691 |
| Citation | Willart MA, et al. (2012) Interleukin-1alpha controls allergic sensitization to inhaled house dust mite via the epithelial release of GM-CSF and IL-33. J Exp Med 209(8):1505-17 |
| abstractText | House dust mite (HDM) is one of the most common allergens worldwide. In this study, we have addressed the involvement of IL-1 in the interaction between HDM and the innate immune response driven by lung epithelial cells (ECs) and dendritic cells (DCs) that leads to asthma. Mice lacking IL-1R on radioresistant cells, but not hematopoietic cells, failed to mount a Th2 immune response and did not develop asthma to HDM. Experiments performed in vivo and in isolated air-liquid interface cultures of bronchial ECs showed that TLR4 signals induced the release of IL-1alpha, which then acted in an autocrine manner to trigger the release of DC-attracting chemokines, GM-CSF, and IL-33. Consequently, allergic sensitization to HDM was abolished in vivo when IL-1alpha, GM-CSF, or IL-33 was neutralized. Thymic stromal lymphopoietin (TSLP) became important only when high doses of allergen were administered. These findings put IL-1alpha upstream in the cytokine cascade leading to epithelial and DC activation in response to inhaled HDM allergen. |
