Table 1.

Effects of IL-19 in nonvascular cell types.

Tissue type	Effect	Species	Source
Immune cells	Th2 response in T cells	h, m	[33, 34, 42]
	Inhibits IFN-γ production in T cells	h	[34]
	Induces IL-4 and IL-13 production in T cells	h	[34]
	Induces IL-10 production in monocytes	h	[43]
	Autoinduces IL-19 expression in PBMC; dendritic cells	h	[43]
	Induce KGF expression in CD8+ T cells	h	[44]
	Suppress cell-mediated immunity in postbypass patients	h	[45]
	Induced production of IL-6; TNF-α in monocytes	m	[46]
	Induced ROS production and apoptosis in monocytes	m	[46]
Skin cells	Expressed in keratinocytes in psoriatic skin	h	[29, 47]
	STAT3 phosphorylation in HaCat keratinocyte cell line	h	[33]
Airway epithelium	HBEC-produced IL-19 induces TNF-α production in THP-1 monocyte line	h	[48]
	Induced apoptosis in lung epithelium cells	h	[49]
Colon epithelium	IL-19 expression is protective against dextran sucrose sodium-induced colitis	m	[50]
Cancer cells	Inhibit proliferation in NIH:OVCAR3 (ovarian carcinoma) cells	h	[51]
	Increase proliferation in oral squamous cell carcinoma cells	h	[52]
	Increase proliferation in breast cancer cells	h, m	[53]
	Induced IL-1β, IL-6, TGF-β, MMP-2, -9, and CXCR4 in 4T1 breast cancer cells in vitro	m	[53]
	Induced fibronectin expression in 4T1 breast cancer cells in vitro	m	[53]
Fetal membranes	Induce IL-6 production	h	[39]
	Inhibit LPS-induced TNF-α production	h	[39]
Liver	Induced ROS production in Huh-7 cell line	h	[49]
Synovial fluid	Inhibits apoptosis in RASC	h	[37]
	Activates STAT3 and induces IL-6 production in RASC	h	[37]
	Induces TNF-α, IL-1β, IL-6, and RANKL in collagen-induced arthritis synovial fibroblasts	r	[54]
Nasal fibroblast	Inhibits IL-4-induced eotaxin expression by SOCS1-dependent mechanism	h	[55]

Abbreviations: HBEC: human bronchial epithelial cell, RASC: rat arthritis synovial cell, h: human, m: mouse, r: rat.