ICAM-1 controls development and function of ILC2

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.

Source: The Journal of Experimental Medicine - August 6, 2018 Category: Internal Medicine Authors: Lei, A.-H., Xiao, Q., Liu, G.-Y., Shi, K., Yang, Q., Li, X., Liu, Y.-F., Wang, H.-K., Cai, W.-P., Guan, Y.-J., Gabrilovich, D. I., Zhou, J. Tags: Innate Immunity and Inflammation Articles Source Type: research