scholarly journals The Polymorphism P315L of Human Toll-Like Receptor 1 Impairs Innate Immune Sensing of Microbial Cell Wall Components

2007 ◽  
Vol 178 (10) ◽  
pp. 6387-6394 ◽  
Author(s):  
Katherine O. Omueti ◽  
Daniel J. Mazur ◽  
Katherine S. Thompson ◽  
Elizabeth A. Lyle ◽  
Richard I. Tapping
2013 ◽  
Vol 168 (7) ◽  
pp. 396-406 ◽  
Author(s):  
V. Sukhithasri ◽  
N. Nisha ◽  
Lalitha Biswas ◽  
V. Anil Kumar ◽  
Raja Biswas

2018 ◽  
Author(s):  
Priya Hari ◽  
Fraser R. Millar ◽  
Nuria Tarrats ◽  
Jodie Birch ◽  
Curtis J. Rink ◽  
...  

ABSTRACTCellular senescence is a stress response program characterised by a robust cell cycle arrest and the induction of a pro-inflammatory senescence-associated secretory phenotype (SASP) that is triggered through an unknown mechanism. Here, we show that during oncogene-induced senescence (OIS), the Toll-like receptor TLR2 and its partner TLR10 are key mediators of senescence in vitro and in murine models. TLR2 promotes cell cycle arrest by regulating the tumour suppressors p53-p21CIP1, p16INK4a and p15INK4b, and regulates the SASP through the induction of the acute-phase serum amyloids A1 and A2 (A-SAA) that, in turn, function as the damage associated molecular patterns (DAMPs) signalling through TLR2 in OIS. Finally, we found evidence that the cGAS-STING cytosolic DNA sensing pathway primes TLR2 and A-SAA expression in OIS. In summary, we report that innate immune sensing of senescence-associated DAMPs by TLR2 controls the SASP and reinforces the cell cycle arrest program in OIS.


2000 ◽  
Vol 28 (5) ◽  
pp. 551-556 ◽  
Author(s):  
S. Akira

The Toll signalling pathway, which is required for establishment of dorsoventral polarity in Drosophila embryos, plays an important role in the response to microbial infections. Recently, Tolllike receptors (TLRs) have also been identified in mammals. TLR4 has been shown to function as the transmembrane component of the lipopolysaccharide receptor, while TLR2 recognizes peptidoglycans from Gram-positive bacteria, lipoproteins and yeast. Although various microbial cell-wall components are recognized by different receptors, all of these responses are abrogated in MyD88-deficient cells. These results show that different TLRs recognize different microbial cell-wall components, and that MyD88 is an essential signalling molecule shared among interleukin-1 receptor/Toll family members.


2020 ◽  
pp. 463-471
Author(s):  
Artur J. Ulmer ◽  
Volker T. El-Samalouti ◽  
Ernst T. Rietschel ◽  
Hans-Dieter Flad ◽  
Roman Dziarski

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