Table 2.

Studies of the roles of NLRP3 inflammasome in autoimmune diseases.

	Effect of NLRP3 inflammasome		Regulation of NLRP3 inflammasome activation and relevant pathway in autoimmune diseases.
	Specific mechanism	Common mechanism	Positive regulation	Negative regulation
IBD	Disrupted inflammasome responses result in dysbiosis and increased colonization of pathobionts (57). .	Physiological condition: sense and respond to foreign milieu in the extracellular environment, via pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), mediate host immune responses to microbial infection and cellular damage. Pathological conditions: 1) Histiocytic and organic inflammation promoted by cytokine IL-1 and IL-18; 2) Induce adaptive immune dysfunction via NLRP3 inflammasome activation, inducing the migration and differentiation of T cell by cytokines; 3) Pyroptosis modulated by activated caspase-1 of immunocyte and specific histocytes.	Transporter 4 (58); Oxazolone (59); Protein tyrosine phosphatase non-receptor 22 (60).	Fasting-mimicking diet (61); Nutrient deprivation (62); CircRNA HECTD1 (63); Naringin (64); Carboxyamidotriazole (65); Growth differentiation factor 11 (66); Phloretin (67); Nuclear factor E2-related factor-2 (68); Cardamonin (69); sDR5-Fc fusion protein (70); Hydrogen sulfide (71); Cinnamaldehyde (72); BBG (a P2X7R blocker) and OLT1177 (73).
Psoriasis	IL-1 participates in pathogenesis partially (74).		CD100/PlxnB2 (75); Tristetraprolin (TTP) downregulation (76); Tumor necrosis factor (TNF)-α (77); Acute-phase protein serum amyloid A (78).	Bay11-7082 (79); Datura Metel L (80).; Cycloastragenol (81); Cas9 RNP nanocomplexes (82).
RA	NLRP3 inflammasome activation contributes to Th1 differentiation in CD4+ T cells (83); Induce Th2 differentiation and antibodies production (84).		TNF-α and calreticulin (85); Calcium-sensing receptor (86); Tofacitinib (87).	MCC950 (88); Protectin DX (89); Taraxasterol (90); Celastrol (91); Punicalagin (92); Hsa_circ_0044235 (93); hUCB-MSCs (94); A20 (44); tristetraprolin (95).
SSC	Downstream factors including IL-1, IL-18, and miR15 promote collagen synthesis and fibrosis (96, 97).		MiR-155 (97); Parvovirus B19 (98).
T1DM	IL-1β induces the migration of proinflammatory cells into pancreatic islets (99, 100); IL-1β has direct cytotoxic effects on beta-cells (99, 100); Autoreactive T cells infiltrate pancreatic islets and cause beta-cell death (101).		LPS+ATP (102); Nitric oxide (103); Metabolic stress (104); Mitochondrial DNA (mDNA) (105).	Verapamil (106); Scutellarin (107); Ginsenoside Rg1 (108); Low-methoxyl pectin (109); fingolimod (110).
SLE	Autoantibodies induce NLRP3 inflammasome activation (82, 111); accumulation of NETs contributes to the pathogenesis (112, 113).		U1-small nuclear ribonucleoprotein (114); Glycogen synthase kinase 3β (115); Cyclic GMP-AMP synthase (116); Neutrophil extracellular traps (NETs) (117); Surface CXCR2 expression (118); Reactive oxygen species (119).	Xenon (120); Honokiol (121); Tris (dibenzylideneacetone) dipalladium (122); Cf-02 (123); Let-7f-5p (124); Magnolol Bay11-7082 (125); Curcumin (126); Melatonin (127); Lcariin (128); Piperine (129); Citral (130).
AITDs			Excessive iodine (131).	Yanghe decoction (132).