Table 1.

Main Transcription Factors (TFs) Regulating Inflammasome Genes.

TF	Context	Target	Species	Outcome
AhR	Xenobiotics, metabolites	Nlrp3	m	Anti-inflammatory
ATF4	ER stress	NLRP1	h	Pro-inflammatory
BLIMP1	Human steady state	AIM2	h	Negative regulation
C/EBPβ	Cell differentiation	MEFV, IL1B, IL1RN	h	Cell-specific expression
CHOP	ER stress	Casp11	m	LPS-induced lung inflammation
CREB	PGE2 signaling	IL1B	h	Pro-inflammatory
GFI1	Negative feedback loop	Nlrp3	m	Anti-inflammatory
HIF1α	Metabolism/Hypoxia	IL1B	h, m	Pro-inflammatory
IRF1	IFN-Υ treatment	CASP1	h, m	Pro-inflammatory
IRF1	IFN-Υ treatment	IL18BP	h	Anti-inflammatory
IRF1/2	IFN-Υ treatment	AIM2	h	Pro-inflammatory
IRF2	Steady state	CASP4	h	Inflammasome competence
IRF2	Steady state	GSDMD	h, m	Inflammasome competence
IRF4	cDC1-steady state	Nlrc4, Il1b, Pycard	m	Antigen presentation
IRF8	cDC2-steady state	Nlrp3, Nlrc4, Pycard, Il1b	m	Antigen presentation
IRF8	BMDM-steady state	Naip2, 5, 6, Nlrc4	m	Resistance to Salmonella
IRF8	EBV + lymphoblastoid cells	CASP1	h	EBV lytic cycle
ISGF3	type I IFN response	Il18	m	LPS-mediated induction
LXRα	Metabolism	IL1B	h	Pro-inflammatory
NF-κB	Pro-inflammatory signals	NLRP3, MEFV, CASP4, CASP5, Casp11, Gsdmd, IL18, IL1B, IL1RN	h, m	Kinetics of inflammasome response
NFAT5	Osmotic stress	Nlrp3	m	Pro-inflammatory
NR1D1	Circadian clock	Nlrp3	m	Circadian oscillation
NRF2	Oxidative stress	Il1b	m	Pro-inflammatory
p53	DNA damage	Casp11, CASP1, NLRC4	m, h	Pro-inflammatory
PU.1	Cell differentiation	IL-18, IL1B, IL1RN	h	Cell-specific expression
SREBP-1A	NF-κB activation	Nlrp1a	m	Metabolic inflammation
STAT1	IFN-Υ treatment	AIM2	h	Induction
STAT1	IFN-Υ treatment	IL18BP	h	Anti-inflammatory
STAT3	IL-10, IL-20R family	Il1b	m	Anti-inflammatory
STAT3	IL-21 in DC	Il1b	m	Resistance to pneumonia Virus of mice

TFs highlighted in gray have a negative effect. See text for details and references. “m” stands for mouse, “h” for human.