TLR signaling pathways.

By K. Takeda, Shizuo Akira. Seminars in Immunology, 2004

2,556 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/2edca456e08c513276b565cca62090186d5c6afc

How researchers see this paper

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

In Cancer Research

1. B. Magnadóttir
2. S. Gordon
3. S. Pun
4. Eric G. Pamer
5. Aly Karsan
6. Baochong Gao
7. M. Tsan
8. Heather H Gustafson

In Immunology

1. S. Gordon
2. F. Martínez
3. Heather H Gustafson
4. S. Pun
5. Chayanon Ngambenjawong
6. B. Magnadóttir
7. Eric G. Pamer
8. Aly Karsan

In Oncology

1. F. Martínez
2. S. Gordon
3. B. Magnadóttir
4. S. Pun
5. Eric G. Pamer
6. Heather H Gustafson
7. Chayanon Ngambenjawong

Citations in the corpus

• The M1 and M2 paradigm of macrophage activation: time for reassessment (2014, background): “As for IFN-g, the numbers of macrophages in TLR KO animals are normal, but their activation is defective and therefore survival to infection is severely impaired; for seminal and recent views, see [29-32].”
• Regulation of plasma-cell development (2005, background): “TLRs signal through activation of nuclear factor-κB (NF-κB) and JUN amino-terminal kinase (JNK”
• Immunological Control of Fish Diseases (2010, background): “Important PRRs are the toll-like receptors (TLRs), which has received some attention in fish research in recent years (Akira and Hemmi 2003; Heine and Lien 2003; Takeda and Akira 2004).”
• Progress in tumor-associated macrophage (TAM)-targeted therapeutics (2017, positive): “interferon regulatory factors (IRFs) and nuclear factor kappaB (NF-κB)) to mount an inflammatory response [24][25].”
• Immune responses to Listeria monocytogenes (2004, background): “At the cell surface, Toll-like receptors (TLRs) transmit signals in response to microbial molecules that activate innate immune defence”
• Paneth cells directly sense gut commensals and maintain homeostasis at the intestinal host-microbial interface (2008, background): “Together, these findings suggest that TLRs, rather than IL-1R or IL-18R, direct expression of the MyD88dependent antimicrobial response.”
• Lipopolysaccharide signaling in endothelial cells (2006, background): “59 Activation of TLR4 leads to stimulation of both a MyD88-dependent and a MyD88-independent pathway”
• Endogenous ligands of Toll‐like receptors (2004, background): “The DD of MyD88 then binds the DD of IL-1R-associated kinase, and the signal is propagated via tumor necrosis factor (TNF) receptor-associated factor-6, leading to the activation of nuclear factor (NF)- B and mitogen-activated protein kinases and the transcription of immunologically relevant genes [”
• The grateful dead: damage‐associated molecular pattern molecules and reduction/oxidation regulate immunity (2007, neutral): “88 (MyD88) and IL-1R-associated kinase (78).”