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. 2020 Oct;55:15–25. doi: 10.1016/j.cytogfr.2020.08.003

Fig. 1.

Fig. 1

Recognition of sterile inflammatory factors by innate cell surface receptors primes NLRP3 for inflammasome activation. A. Sensing of priming signals regulate NLRP3 at different levels 1) transcriptional, 2) post-transcriptional and 3) post-translational prior to the second or activating step. Nuclear factor-κB (NF-κB); reactive oxygen species (ROS); sensor (NOD)-like receptor protein 3 (NLRP3); apoptosis-associated speck-like protein containing a CARD (ASC); Interleukin (IL); tristetraprolin (TTP). B. Sterile priming stimuli act upon a wide variety of cell surface receptors, with the same stimuli being able to target different receptors. Sphingosine-1-phosphate (S1P) receptor 1 (S1PR1); advanced glycation end product (AGE); receptor for AGEs (RAGE); free fatty acid (FFA); oxidised low density lipoprotein (oxLDL); toll like receptor 4 (TLR4); serum amyloid A (SAA); cluster of differentiation 36 (CD36); saturated fatty acid (SFA); toll like receptor 2 (TLR2); complement component 5a (C5a) receptor (C5aR); Interleukin-6 (IL-6) receptor (IL-6R); Interleukin-1 (IL-1) receptor 1 (IL-1R1); tumour necrosis factor-α (TNF-α) receptor 1 (TNFR1).