Acidic Mammalian Chitinase in Asthmatic Th2 Inflammation and IL-13 Pathway Activation

By Zhou Zhu, T. Zheng, R. Homer, Yoon-Keun Kim, Ning-yuan Chen, L. Cohn, Q. Hamid, J. Elias. Science, 2004

854 citations recorded by the source corpus.

Subfields: Immunology, Insect Science, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/878e2b9c7f05654cb4ab454d1eaa0026d885dce3

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In Immunology

1. TA Wynn
2. A. Mantovani
3. A. Sica
4. P. Murray
5. D. Mosser
6. J. Edwards
7. H. Hammad
8. B. Lambrecht

In Molecular Biology

1. A. Sica
2. P. Murray
3. Luke Barron
4. A. Mantovani
5. T. Ramalingam
6. TA Wynn
7. B. Lambrecht
8. S. Hogan

Citations in the corpus

• Arginase-1–Expressing Macrophages Suppress Th2 Cytokine–Driven Inflammation and Fibrosis (2009, background): “characterize AAMs [19,42], in addition to analyzing the function”
• Macrophages: Master Regulators of Inflammation and Fibrosis (2010, background): “Neutralization of AMCase activity has been shown to ameliorate Th2-dependent inflammation, AAMw development, airway remodeling, and airway hyperresponsiveness in an aeroallergen asthma model, in part by inhibiting activation of the IL-13 pathway.(131) A similar effect was also recently ascribed to t”
• The cytokine network in asthma and chronic obstructive pulmonary disease. (2008, neutral): “expression of acid mammalian chitinase (AMC) (11).”
• Exploring the full spectrum of macrophage activation (2008, background): “43 ), acidic mammalian chitinase (AMCase) and stabilin-interacting chitinase-like protei”
• Role of Chitin and Chitinase/Chitinase-Like Proteins in Inflammation, Tissue Remodeling, and Injury (2011, background): “AMCase regulates innate (7) and adaptive (5) Th2 inflammatory and remodeling responses.”
• Macrophage plasticity and polarization: in vivo veritas. (2012, positive): “Evidence now indicates that chitin- and arginase-dependent M2 pathways play an active role in pathogenesis (75, 76).”
• Interleukin‐13 in asthma pathogenesis (2004, background): “In an elegant paper, Zhu and colleagues (92) have shown that IL-13 induces the expression of an AMCase in airway epithelium and macrophages and that either inhibition of chitinase enzyme activity or treatment of mice with antiserum directed against the chitinase abolished IL-13-induced AHR.”
• Integrating mechanisms of pulmonary fibrosis (2011, background): “, 2003), chitinase family members (Zhu et al., 2004; Lee et al., 2009), chemokines (Belperio et al.”
• Dendritic cells and epithelial cells: linking innate and adaptive immunity in asthma (2008, background): “Chitinases have also been implicated in causing T H 2-cell immune responses by inducing the production of CCL2 and CCL11 by epithelial cells, and the levels of acidic mammalian chitinase are increased in the airways of asthmatic”
• Eosinophils: Biological Properties and Role in Health and Disease (2008, background): “…al. 1990a; Moser et al. 1992; Horie et al. 1997), adhesion molecules (e.g., b1, b2, and b7 integrins) (Bochner & Schleimer 1994), chemokines such as RANTES and the eotaxins (Zimmermann et al. 2003), and other recently identified molecules (e.g., acidic mammalian chitinase) (Zhu et al. 2004) (Fig.”
• INTERLEUKIN-4- AND INTERLEUKIN-13-MEDIATED ALTERNATIVELY ACTIVATED MACROPHAGES: ROLES IN HOMEOSTASIS AND DISEASE (2013, neutral): “Yet, although both Ym2 and AMCase are highly upregulated in a STAT6-dependent manner during helminth infection, lung-specific transgenic expression of either AMCase or Ym2 in Balb/c mice did not result in spontaneous lung inflammation (25; T. Reese and R. Locksley, unpublished observations), indicat”