Table 2.

The list of transitions of the model.

Transition	Biological Meaning	References	Transition	Biological Meaning	References
$t_0$	induction cell-mediated immunity	[23]	$t_{35}$	IRAK4 recruitment	[24]
$t_1$	INF-$\gamma$ synthesis influencing	[23]	$t_{36}$	connection with IRAK1 and its phosphorylation	[24]
$t_2$	infection modulation	[23]	$t_{37}$	TRAF6 recruitment and binding to IRAK1	[24]
$t_3$	classical macrophages activation by INF-$\gamma$	[3,23]	$t_{38}$	IRAK1P-TRAF6 dissociation	[24]
$t_4$	pro IL-18 synthesis	[3]	$t_{39}$	TAK1-TAB2 phosphorylation	[24]
$t_5$	modulation by TNF	[3]	$t_{40}$	TRAF6-TAK1P-TAB2P-TAB1 complex translocation to cytosol	[24]
$t_6$	modulation by INF-$\gamma$	[3,23]	$t_{41}$	TRAF6 ubiquitination	[24]
$t_7$	pro IL-18 activation by caspase 1 enzymatic cleavage	[3]	$t_{42}$	IKK complex phosphorylation	[24,28,33]
$t_8$	IL-18 and IL-18Rs binding	[3]	$t_{43}$	p38 and MAPK signalling pathway	[28]
$t_9$	nitric oxide synthesis	[30]	$t_{44}$	RIP1 recruites TAK1 via TAB2	[29]
$t_{10}$	cardiac contractile dysfunction	[30]	$t_{45}$	RIP1 ubiquitination	[29]
$t_{11}$	cardiovascular disease (CVD)	[30]	$t_{46}$	TRAF2 ubiquitination	[29]
$t_{12}$	IFR1 synthesis	[25]	$t_{47}$	forming TRAF2-TRADD- RIP1-TRAF5 complex	[29]
$t_{13}$	JAK and STAT pathway activation	[23,25]	$t_{48}$	TNFR1 trimerization	[27,29]
$t_{14}$	INF-$\gamma$-IFNRs interaction	[23,25]	$t_{49}$	usage	[27]
$t_{15}$	reaction catalysed by NADPH oxydase	[26,30]	$t_{50}$	TNFR1 stabilization	[27]
$t_{16}$	lipids peroxydation	[26,30]	$t_{51}$	SODD expression	[27]
$t_{17}$	neighboring endothelial cells stimulation	[3,26]	$t_{52}$	TNFR1 endocytosis	[29]
$t_{18}$	neovascularization inhibition	[3]	$t_{53}$	FADD recruitment	[29]
$t_{19}$	FasL expression on inflammatory cells	[3]	$t_{54}$	pro caspase 8 recruitment	[29]
$t_{20}$	ICAM1 and VCAM1 up regulation	[3]	$t_{55}$	connection through DDs	[29]
$t_{21}$	ICAM1 increasing	[30]	$t_{56}$	ubiquitylation and degradation	[28,33]
$t_{22}$	VCAM1 decreasing	[30]	$t_{57}$	phosphorylation cascade initiation	[28,33]
$t_{23}$	hemodialysis (HD)	[31]	$t_{58}$	I$\kappa$B dissociation from the complex	[28,33]
$t_{24}$	attracting monocytes	[26]	$t_{59}$	p50–p65 translocation to the nucleus	[28,33]
$t_{25}$	transformation into macrophages	[26]	$t_{60}$	MCP1 gene transcription	[28]
$t_{26}$	activation	[26]	$t_{61}$	VCAM1 transcription	[26,28]
$t_{27}$	transformation into foamy cells	[26,30]	$t_{62}$	ICAM1 transcription	[28]
$t_{28}$	atherosclerotic plaque	[26]	$t_{63}$	TNF gene transcription	[28,29]
$t_{29}$	severe inflammation	[3,32]	$t_{64}$	iNOS gene transcription	[28,30]
$t_{30}$	LPS and LBP binding	[32]	$t_{65}$	proinflammatory response	[28,29,30]
$t_{31}$	LPS presentation to TLR4 and CD14	[32]	$t_{66}$	no apoptosis	[28,29]
$t_{32}$	TLR4 and MyD88 connection	[24]	$t_{67}$	caspase 8 autocleavage and activation	[29]
$t_{33}$	MyD88 recruitment	[24]	$t_{68}$	caspase 3 activation	[29,31]
$t_{34}$	active IL-18-IL-18Rs ($\alpha$ and $\beta$) and MyD88 connection	[3]	$t_{69}$	apoptosis enhancement	[29,31]