Inflammasomes are multi-protein complexes whose activity has been implicated in physiological and pathological inflammation. The hallmarks of inflammasome activation are the secretion of the mature forms of caspase-1 and interleukin-1β (IL-1β) from cells of the innate immune system.
AdipoGen provides a large selection of research reagents targeted to the various components of the inflammasome, thanks to a long-term collaboration with the Professor Jürg Tschopp group – the team who discovered the inflammasome in 2002.
Standard Inflammasome Signalling Antibodies
NOD-Like Receptors (NLRs):
anti-NAIP1/2/5 (mouse), mAb (Naipa-1)
anti-NLRP1/NALP1 (human), pAb (AL176)
anti-NLRP3/NALP3, mAb (Cryo-2)
anti-NLRP3/NALP3 (mouse), mAb (Cryo-1)
anti-NLRP6/NALP6 (human), mAb (Clint-1)
anti-Nod1 (human), pAb (AL184)
RIG-like Helicases (RLHs) – Antiviral Signaling:
anti-RIG-I, mAb (Alme-1)
anti-RIG-I, mAb (Alme-1) (Biotin)
anti-Cardif (human), mAb (Adri-1)
anti-MDA5 (human), mAb (Hely-1)
anti-NS3 (HCV), mAb (1B6)
anti-NS5B (HCV), mAb (5B-3B1)
anti-NS5B (HCV), mAb (blocking) (5B-12B7)
Cytosolic DNA Sensor:
Signalling Antibodies:
anti-Asc [Pycard], pAb (AL177)
anti-Asc [Pycard], pAb (AL177) (preservative free)
anti-Asc, pAb (AL177) (ATTO 647N)
anti-Pyrin (human), pAb (AL196)
anti-TRAM (human), pAb (AL239)
Cytosolic PAMPs Sensors:
anti-Caspase-4/11 (p20), mAb (Flamy-1)
anti-Caspase-4/11 (p20), mAb (Flamy-1) (Biotin)
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Background Information
An inflammasome represents a high molecular weight complex that activates inflammatory caspases and cytokines of the IL-1 family (IL-1β, IL-18 and depending on the stimulus also IL-1α). Several inflammasomes have been described which contain different sensor proteins such as NLRP1 (NALP1), NLRP3 (NALP3), IPAF (NLRC4), NLRP6 (NALP6), NLRP12 (NALP12), RIG-I and AIM-2 (absent in melanoma 2). Most of these inflammasomes require the adapter protein Asc (apoptosis-associated speck-like protein containing a caspase recruitment domain) to recruit caspase-1 to the inflammasome complex. Upon binding to the inflammasome, caspase-1 is cleaved and activated, leading to cleavage of its various targets and causing maturation and secretion of the pro-inflammatory IL-1β.
Inflammasomes can be activated through multiple signals including live bacteria, microbial toxins, xeno-compounds, particulates cytoplasmic pathogen-associated molecular patterns (PAMPs) and/or endogenous danger signals (DAMPs). Inflammasome activity has been causally linked to the induction of numerous inflammatory responses, which can be either beneficial or harmful to the organism. Beneficial responses arise by maintaining homeostatic tissue function (detection and repair of tissue damages after trauma or pathogen invasion). Among the harmful inflammatory responses are particle-induced sterile inflammation, caused by host-derived particles such as monosodium urate (MSU) crystals, which are involved in the pathogenesis of gout, as well as environmental and industrial particles such as asbestos, silica and metallic nanoparticles, which induce lung inflammation upon inhalation. Accumulating evidence also implicates inflammasome activity in numerous other diseases, including cancer and the development of metabolic diseases (like type 2 diabetes, atherosclerosis), some neurodegenerative diseases (like Alzheimers, Prion and Parkinson’s Disease), autoimmune diseases (such as multiple sclerosis) and inflammatory bowel diseases. Beneficial effects for the host include the enhancement of vaccine efficacy.
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