Review Article

Anti-Inflammatory Effects of Interleukin-19 in Vascular Disease

Table 1

Effects of IL-19 in nonvascular cell types.

Tissue typeEffectSpeciesSource

Immune cellsTh2 response in T cellsh, m[33, 34, 42]
Inhibits IFN- production in T cellsh[34]
Induces IL-4 and IL-13 production in T cellsh[34]
Induces IL-10 production in monocytesh [43]
Autoinduces IL-19 expression in PBMC; dendritic cellsh [43]
Induce KGF expression in CD8+ T cellsh[44]
Suppress cell-mediated immunity in postbypass patientsh[45]
Induced production of IL-6; TNF- in monocytesm [46]
Induced ROS production and apoptosis in monocytesm [46]

Skin cellsExpressed in keratinocytes in psoriatic skinh[29, 47]
STAT3 phosphorylation in HaCat keratinocyte cell lineh[33]

Airway epitheliumHBEC-produced IL-19 induces TNF-α production in THP-1 monocyte lineh[48]
Induced apoptosis in lung epithelium cellsh[49]

Colon epitheliumIL-19 expression is protective against dextran sucrose sodium-induced colitism[50]

Cancer cellsInhibit proliferation in NIH:OVCAR3 (ovarian carcinoma) cellsh[51]
Increase proliferation in oral squamous cell carcinoma cellsh[52]
Increase proliferation in breast cancer cellsh, 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 membranesInduce IL-6 productionh[39]
Inhibit LPS-induced TNF-α productionh[39]

LiverInduced ROS production in Huh-7 cell lineh[49]

Synovial fluidInhibits apoptosis in RASCh[37]
Activates STAT3 and induces IL-6 production in RASCh[37]
Induces TNF-α, IL-1β, IL-6, and RANKL in collagen-induced arthritis synovial fibroblastsr[54]

Nasal fibroblastInhibits IL-4-induced eotaxin expression by SOCS1-dependent mechanismh [55]

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