Neutrophil plasticity enables the development of pathological microenvironments: implications for cystic fibrosis airway disease

Molecular and Cellular Pediatrics

Table 1 Direct targets of NE-dependent regulation

Immunological targets
Activated by cleavage	Inhibited by cleavage
Arginase-1 [106]	CD2/CD4/CD8 [107]
Chemerin [161]	CD14 [162]
IL-36 receptor antagonist [163]	CD16 [164]
IL-8 [84]	CD43 [165]
MMP-9 [67]	CCL3 [166]
PAR-1/PAR-2 [167, 168]	Complement factors [169–172]
Pro-IL-1β [173]	CXCL12 [174]
Transient receptor potential vanilloid 4 [67]	CXCR1 [82]
Tumor growth factor α [175]	IgA [70] and IgG [71, 72]
	IL-2 receptor [108]
	IL-6 [176, 177]
	IL-8 [86]
	PAR-3 [168]
	Progranulin [178, 179]
	TIMP-1/TIMP-2/TIMP-3 [180, 181]
Non-immunological targets
Activated by cleavage	Inhibited by cleavage
α₂β₃ integrins [182]	Cadherins [183]
EGFR [184]	Elastin [185]
ENaC [186, 187]	Ferritin [188]
	Fibrin stabilizing factor XIII [189]
	Surfactant protein A [190]
	Surfactant protein D [191]
	Vascular endothelial growth factor [192]

EGFR epidermal growth factor receptor, ENaC epithelial sodium channel, PAR protease-activated receptor, TIMP tissue inhibitor of metalloproteinase