Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer.

By M. Karin, T. Lawrence, V. Nizet. Cell, 2006

1,018 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1bc320912778de54297e8c24deef320aec280bf6

How researchers see this paper

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

In Immunology

1. M. Karin
2. A. Mantovani
3. R. Medzhitov
4. S. Grivennikov
5. D. Artis
6. T. Lawrence
7. Subhra K. Biswas
8. R. Flavell

In Molecular Biology

1. R. Medzhitov
2. E. White
3. M. Karin
4. A. Mantovani
5. S. Grivennikov
6. T. Lawrence
7. Lan Lin
8. Jianqiong Zhang

Citations in the corpus

• Role of autophagy in cancer (2007, background): “In contrast to apoptosis, necrosis and cell lysis causes nuclear HMGB1 to be released from cells, and this and other events stimulate the innate immune response, the recruitment of inflammatory cells, cytokine production and nuclear factor-κB ( NFκB ) activation, which in some cases is linked to i”
• Microglia-mediated neurotoxicity: uncovering the molecular mechanisms (2007, background): “Recently, PRRs have been linked to numerous diseases of chronic inflammation such as Crohn's disease, arthrosclerosis, diabetes and cance”
• Dual Roles of Immune Cells and Their Factors in Cancer Development and Progression (2011, background): “TNF itself also plays an essential role in several models of cancer, and is a critical inflammatory mediator in many autoimmune diseases of both mice and humans primarily acting via induction of NF-κB (5, 6).”
• Epithelial-cell recognition of commensal bacteria and maintenance of immune homeostasis in the gut (2008, background): “The necessity to regulate immune responses to commensal bacteria is exemplified by evidence that dysregulation of the balance between tolerance and immunity can contribute to the pathogenesis of numerous inflammatory conditions, including food allergies, inflammatory bowel disease (IBD) and intestin”
• Interleukin-22 but not interleukin-17 provides protection to hepatocytes during acute liver inflammation. (2007, background): “Chronic inflammation is also linked to the development of cancer (Karin et al., 2006).”
• Inflammation in wound repair: molecular and cellular mechanisms. (2007, background): “through which macrophages sense and respond to their microenvironment, including Toll-like receptors, complement receptors, and Fc receptors (Gordon 2003; Karin et al., 2006).”
• The nuclear factor NF-kappaB pathway in inflammation. (2009, background): “However, there is some suggestion that endogenous ligands may trigger TLRs during tissue injury and certain disease states, which may act to promote inflammation in the absence of infection (Karin et al. 2006).”
• Role of intestinal microbiota and metabolites on gut homeostasis and human diseases (2017, background): “Impaired epithelial integrity is demonstrated to activate the resident inflammatory cells in response to pathogenic invaders or endogenous ligands, which, coupled with a failure of normal regulatory mechanisms that limit leukocyte activation, would initiate a cascade leading to chronic inflammation ”
• Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer (2009, background): “However, the functions of NF-κB and STAT3 extend far beyond the cancer cell and both transcriptional factors are important regulators of immune and inflammatory functions (9,10).”
• Elicitors, effectors, and R genes: the new paradigm and a lifetime supply of questions. (2007, background): “Animal innate immunity must be down-regulated at topologically exterior surfaces including the lung and gut epithelia (90).”
• IL-6 and STAT3 are required for survival of intestinal epithelial cells and development of colitis associated cancer (2009, background): “The tumor-promoting effect of inflammation is now widely recognized and better understood (Coussens and Werb, 2002; Karin et al., 2006 ).”
• Origin and physiological roles of inflammation (2008, background): “The pathological potential of inflammation is unprecedented for a physiological proces”