Signaling by Toll-Like Receptor 2 and 4 Agonists Results in Differential Gene Expression in Murine Macrophages

By M. Hirschfeld, J. Weis, V. Toshchakov, C. Salkowski, M. J. Cody, D. Ward, N. Qureshi, S. Michalek, S. Vogel. Infection and Immunity, 2001

751 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Microbiology

View Paper: https://www.semanticscholar.org/paper/457329daca0f54393b906b028210095c972b2a5e

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. Shizuo Akira
2. Luke A. O'Neill
3. Taro Kawai
4. K. Takeda
5. R. Medzhitov
6. O. Takeuchi
7. T. Kaisho
8. Shintaro Sato

In Immunology

1. Shizuo Akira
2. R. Medzhitov
3. Taro Kawai
4. O. Takeuchi
5. K. Takeda
6. Luke A. O'Neill
7. T. Kaisho
8. Satoshi Uematsu

In Microbiology

1. Shizuo Akira
2. R. Medzhitov
3. K. Takeda
4. Taro Kawai
5. O. Takeuchi
6. Gordon D. Brown
7. Mihai G. Netea
8. T. Fujita

Citations in the corpus

• Toll-like receptors in innate immunity. (2004, neutral): “In addition, TLR2 reportedly recognizes LPS preparations from non-entero-bacteria such as Leptospira interrogans, Porphyromonas gingivalis and Helicobacter pyroli (7–9).”
• Dendritic cell lineage, plasticity and cross-regulation (2001, background): “However, LPS from Porphyromonas gingivalis does not stimulate CD8 + DCs to produce IL-12 and preferentially induces a T H 2 respons”
• An integrated model of the recognition of Candida albicans by the innate immune system (2008, background): “By contrast, several studies have demonstrated that although TLR2 ligation can induce pro-inflammatory cytokines, this effect is weaker than that mediated by TLR4 ligatio”
• The Interleukin-1 Receptor/Toll-Like Receptor Superfamily: Signal Transduction During Inflammation and Host Defense (2000, methodology): “The LPS used in these studies was derived from Escherichia coli; however, researchers have demonstrated that responses to Porphyromonas gingivalisderived LPS are only partially impaired in TLR-4-deficient macrophages (100), suggesting that a receptor other that TLR-4 is involved in recognition of so”
• Lipopolysaccharide Stimulates the MyD88-Independent Pathway and Results in Activation of IFN-Regulatory Factor 3 and the Expression of a Subset of Lipopolysaccharide-Inducible Genes1 (2001, result): “Consistent with our result, Hirschfeld et al. ( 42 ) recently showed that macrophage stimulation by Porphyromonas gingivalis LPS preparation, a potent TLR2 ligand, resulted in diminished IP-10 expression compared with stimulation by E. coli LPS.”
• Innate immune recognition. (2002, background): “The list includes peptidoglycan (73, 77), bacterial lipoproteins (78–80), a phenol soluble factor from Staphylococcus epidermidis (81), LPS from Prophyromonas gingivitis (82) andLeptospira interrogans(which differs in structure from the LPS of gram-negative bacteria) (83), glycosylphosphotidylinosit”