Table 1. Senescence-inducing cytokines and signaling molecules: cell systems and properties.

Cytokine	Cell system	Mechanisms	References
IFNβ	IMR90, IMR90+H-RasV12E	DDR, ATM, p53-dependent senescence	73
Constitutively active STAT5	IMR90 BJ, IMR90	DDR, ATM, Chk2, p53 PML, reduced Myc, Rb	83 and 84
IGFBP5	HUVEC atherosclerotic lesion	DDR, p53-dependent senescence IGFBP5 detected	63
IL-6/sIL-6Rα	TIG3-BRAFV600E	IL-6, induced by BRAFV600E-C/EBPβ, reinforce H-RasV12E-dependent senescence. IL-8 is also involved.	22
CXCR2	IMR90+MEK:ER	MEK-induced CXCR2 reinforce MEK-dependent senescence	23
IFNβ	Genotoxic drug-treated tumor cells BJ	JAK/STAT-mediated PML1 induction contributes to drug-induced senescence	26 and 27
IL-6/sIL-6Rα	TIG3	STAT3-IGFBP5 axis forms a senescence-inducing circuit involving ROS, DDR, p53, RelA and IL-6	11
IL-1β+TGFβ	BJ	Secreted IL-1β+TGFβ induces senescence through increasing Nox4	76
IL-22	Hepatic stellate cells	STAT3-SOCS3 induces senescence and inhibits liver fibrosis. SOCS3 activates p53 by binding to p53.	32
IFNβ	HPV-transformed keratinocytes	JAK/STAT-induced PML together with p53 and p21CIP1 involved in IFNβ−induced senescence	28
TNFα+IFNγ	SV40-Tag-transformed β cell	Th1 cells specific to SV40 Tag causes senescence of target cells through STAT1, TNFR1, p16INK4a-dependent mechanism	75