Fibrotic disease and the T(H)1/T(H)2 paradigm.

By TA Wynn. Nature reviews. Immunology, 2004

878 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/5c3d521a8522f12d17ffb7e8031a713d18843f00

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

1. A. Mantovani
2. TA Wynn
3. A. Sica
4. Subhra K. Biswas
5. M. Locati
6. M. Galdiero
7. M. Wilson
8. J. Allen

Citations in the corpus

• Evolutionary Causes and Consequences of Immunopathology (2005, background): “For example, influenza induces much more immunological activity than is necessary to clear the virus, and it is the excess that does most of the damage to the lung (Hussell et al. 2001, Xu et al. 2004).”
• Hypertrophic Scarring and Keloids: Pathomechanisms and Current and Emerging Treatment Strategies (2011, background): “While the development of a Th2 response (with production of interleukin [IL]-4, IL-5, IL-10 and IL-13) has been strongly linked to fibrogenesis, a predominance of Th1 CD41 cells has been shown to almost completely attenuate the formation of tissue fibrosis via production of interferon-γ (IFN-γ) and ”
• Mechanisms of fibrosis: therapeutic translation for fibrotic disease (2012, unknown): “72), and although all three have been linked to the development of fibrosis 55,73,74 , IL-13 has emerged as a dominant mediator of fibrotic tissue remodeling in several experimental and natural models of fibrosis 74 .”
• Intratumor T helper type 2 cell infiltrate correlates with cancer-associated fibroblast thymic stromal lymphopoietin production and reduced survival in pancreatic cancer (2011, background): “We hypothesized that tumorresident DCs are conditioned by factors released by tumor cells or tumor stroma to favor, in the draining LNs, differentiation of tumor-specific Th2 cells, which then home to the tumor and possibly contribute to disease progression by interacting with other immune and nonim”
• Integrating mechanisms of pulmonary fibrosis (2011, background): “IFN- inhibits fibrosis, whereas the Th2-associated cytokines IL-4, IL-5, and IL-13 have been causally linked to the development of fibrosis in a variety of chronic inflammatory diseases (Wynn, 2004).”
• Macrophages: Master Regulators of Inflammation and Fibrosis (2010, background): “Still others have proposed that AAMw are needed for the activation of collagen-producing myofibroblasts, suggesting a positive feedback loop exists between these two cell types.(76,89,102) Given the presumably important contribution of AAMw to the development of fibrosis, a great deal of recent rese”
• IL-13 signaling through the IL-13α2 receptor is involved in induction of TGF-β1 production and fibrosis (2006, background): “Wu, Z. et al. AP-1 complexes mediate oxidized LDL-induced overproduction of TGFbeta(1) in rat mesangial cells.”
• Pathogenetic mechanisms in radiation fibrosis. (2010, background): “and plasma cells before bladder fibrosis develops [22].”
• Arginase-1–Expressing Macrophages Suppress Th2 Cytokine–Driven Inflammation and Fibrosis (2009, background): “Because hepatic fibrosis, portal hypertension, and variceal bleeding are the primary causes of morbidity and mortality in human schistosomiasis [33], our research has focused on understanding the mechanisms regulating the development of chronic Th2-associated pathology [2].”
• Macrophage plasticity and polarization in tissue repair and remodelling (2013, background): “Parasites represent a paradigm for the role of Th2-driven antimicrobial resistance and for tissue remodelling and fibrosis as an encapsulation strategy [45,102].”