IL-33 Drives Monocyte Recruitment to Lung Interstitium through Chemokine Upregulation
Year: 2017
Type: article
Abstract: mice have a defect in monocyte extravasation from the vasculature to the lung interstitium during induction of type 2 inflammatory responses. This result suggests that monocyte migration to the lungs is IL-33 dependent, and we found that administration of exogenous recombinant IL-33 is sufficient to restore monocyte localization to the lung interstitium. Further investigation of the effect of early administration of recombinant IL-33 on the lungs identified upregulation of multiple chemokines including the monocyte chemoattractants CCL2, CCL7, and CCL22. Importantly, blockade of G-protein coupled receptor-dependent signaling, and thereby chemokine receptor activity, inhibited IL-33-driven monocyte recruitment. CCR2 deficiency prevented recruitment of monocytes to the lung extravascular space during allergic sensitization, and resulted in reduced eosinophilia after allergen challenge. Thus, IL-33 plays a critical role in the initiation of type 2 inflammatory responses by inducing upregulation of chemokines that promote monocyte recruitment to the lung interstitium.
Source: ImmunoHorizons
Institutions: University of Chicago, University of Pittsburgh
Language: English
Topic: IL-33, ST2, and ILC Pathways
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $1,700
Awards: Medical Scientist National Research Service Award, IRF4+ respiratory dendritic cells in type 2 inflammatory responses, Dendritic cell produced IL-33 in Th2 responses, Functional Genomics of IL-33 expression and asthma risk, Cancer Center Support Grant, Immunoregulatory Mechanisms of IL-33 in Heart Transplantation, IRF4+ respiratory dendritic cells in type 2 inflammatory responses
OpenAlex ID: W2750154072