Toll-like receptors control activation of adaptive immune responses

By M. Schnare, G. Barton, Agnieszka Czopik Holt, K. Takeda, Shizuo Akira, R. Medzhitov. Nature Immunology, 2001

1,537 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/63526fb55d62a9c1fa54722d31d728f63b3a446e

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. R. Medzhitov
3. K. Takeda
4. T. Mogensen
5. G. Barton
6. T. Kaisho
7. Jacques Deguine
8. J. Tschopp

In Immunology

1. Shizuo Akira
2. R. Medzhitov
3. T. Mogensen
4. K. Takeda
5. Taro Kawai
6. G. Barton
7. J. Tschopp
8. T. Kaisho

Citations in the corpus

• Cutting Edge: Inflammasome Activation by Alum and Alum’s Adjuvant Effect Are Mediated by NLRP31 (2008, result): “The analysis of CFA adjuvanticity in mice deficient in both TLR signaling and inflammasome activation may shed light on the contribution of each pathway to the immune response during vaccination and may provide an explanation for the contrasting results that have been reported regarding the role of ”
• Cutting Edge: Alum Adjuvant Stimulates Inflammatory Dendritic Cells through Activation of the NALP3 Inflammasome (2008, background): “tive in mounting Th1 and B cell responses (4), this notion”
• Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock (2003, background): “tigen-specific Th1 immune responses (469), whereas the absence of TLR4 affected Th2 responses (77).”
• Lipopolysaccharide-enhanced, Toll-like Receptor 4–dependent T Helper Cell Type 2 Responses to Inhaled Antigen (2002, background): “Although recent studies in MyD88-deficient mice support a role for TLRs in the generation of Th1 responses to proteins, Th2 responses were shown to be MyD88 independent, suggesting TLR signaling is not important for the induction of Th2 cells (7).”
• IRAK-M is a negative regulator of Toll-like receptor signaling. (2002, background): “…the adaptive immune system by the production of proinflammatory cytokines such as IL-1 , IL-6, TNF , or IL-12 and the induction of key surface molecules, which drive T cell activation, including MHC, CD40, CD80, and CD86 (Akira et al., 2001; Medzhitov and Janeway, 1997; Schnare et al., 2001).”