IL-33 Amplifies the Polarization of Alternatively Activated Macrophages That Contribute to Airway Inflammation1
By M. Kurowska-Stolarska, B. Stolarski, P. Kewin, G. Murphy, C. Corrigan, S. Ying, N. Pitman, A. Mirchandani, Batika M. J. Rana, N. Van Rooijen and 5 more. Journal of Immunology, 2009
729 citations recorded by the source corpus.
Subfields: Immunology, Surgery
View Paper: https://www.semanticscholar.org/paper/426c6c9a481f9b770c33291c5848d1d51cec6a77
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Citations in the corpus
- Alternative activation of macrophages: mechanism and functions. (2010, background): “IL-33, a Th2 cell product, binds to ST2L, a subunit of the IL-33 receptor, to amplify Th2 cytokine production and AAM induction (Kurowska-Stolarska et al., 2009).”
- Microglial M1/M2 polarization and metabolic states (2016, background): “Other cytokines induce M2 polarization such as IL-3 (Kuroda et al., 2009), IL-21 (Pesce et al., 2006) and IL-33, (Kurowska-Stolarska et al., 2009) as well as the chemokines, CCL2 and CXCL4 (Roca et al., 2009; Gleissner et al., 2010).”
- INTERLEUKIN-4- AND INTERLEUKIN-13-MEDIATED ALTERNATIVELY ACTIVATED MACROPHAGES: ROLES IN HOMEOSTASIS AND DISEASE (2013, positive): “Accordingly, macrophage depletion or deficiency during type 2 inflammation induced by IL-33, chitin, or helminth infection results in reduced recruitment of eosinophils (25, 117, 118).”
- Macrophage plasticity, polarization, and function in health and disease (2018, background): “airways of patients with atopic dermatitis and asthma which correlated with disease severity (Kurowska-Stolarska et al., 2009).”