| First Author | Lei AH | Year | 2018 |
| Journal | J Exp Med | Volume | 215 |
| Issue | 8 | Pages | 2157-2174 |
| PubMed ID | 30049704 | Mgi Jnum | J:266046 |
| Mgi Id | MGI:6201915 | Doi | 10.1084/jem.20172359 |
| Citation | Lei AH, et al. (2018) ICAM-1 controls development and function of ILC2. J Exp Med 215(8):2157-2174 |
| abstractText | Group 2 innate lymphoid cells (ILC2s) are emerging as key players in the pathogenesis of allergic airway inflammation. The mechanisms regulating ILC2, however, are not fully understood. Here, we found that ICAM-1 is required for the development and function of ILC2. ICAM-1-deficient (ICAM-1(-/-) ) mice displayed significantly lower levels of ILC2s in the bone marrow and peripheral tissues than wild-type controls. CLP transfer and in vitro culture assays revealed that the regulation of ILC2 by ICAM-1 is cell intrinsic. Furthermore, ILC2s from ICAM-1(-/-) mice were functionally impaired, as indicated by the diminished production of type-2 cytokines in response to IL-33 challenge. The reduction in lung ILC2s caused a clear remission of airway inflammation in ICAM-1(-/-) mice after administration of papain or Alternaria alternata. We further demonstrate that ILC2 defects caused by ICAM-1 deficiency are due to ERK signaling-dependent down-regulation of GATA3 protein. Collectively, these observations identify ICAM-1 as a novel regulator of ILC2. |
