IL-20: biological functions and clinical implications

Abstract

SummaryIL-20 belongs to the IL-10 family and plays a role in skin inflammation and the development of hematopoietic cells. Little is known about its other biological functions and clinical implications, however.

A novel transcript of mouse interleukin-20 receptor acts on glomerular mesangial cells as an aggravating factor in lupus nephritis

“…Accumulating evidence has revealed the association of IL-19, [8][9][10][11][12] IL-20 [13][14][15][16][17][18][19][20] and IL-24 [21][22][23][24][25][26] with diseases. To explore if any soluble receptors of these cytokines could function as antagonists of the cytokines, we tried to isolate the alternative spliced transcripts of the receptors for IL-19, IL-20 and IL-24.…”

“…In response to ligand binding, the CRF2 proteins form heterodimers, leading to cytokine-specific cellular responses. The biological effects of these three cytokines appear quite distinct: immune activity with IL-19, [7][8][9][10][11][12] skin biology, atherosclerosis and synovial biology in rheumatoid arthritis with IL-20, [13][14][15][16][17][18][19][20] and tumor apoptosis with IL-24. [21][22][23][24][25][26] Within the CRF2 family, only IL-22 binding protein was identified as a decoy receptor functioning as a naturally occurring, highly specific IL-22 antagonist in both humans [27][28][29] and mice.…”

IL-20 Receptor 2 Signaling Down-Regulates Antigen-Specific T Cell Responses

“…rIL-20 and rIL-24 might promote angiogenesis (12,13). IL-19 was reported to up-regulate Th2 cytokines in an animal model of asthma (14).…”

Pathogenesis of Psoriasis: The Role of Pro-Inflammatory Cytokines Produced by Keratinocytes

“…It was also reported that IL-20 induced IL-6 and TNFin monocytes, stimulated the expression of keratinocytes growth factor (KGF), IL-6, TNFand reactive oxygen species (ROS) in CD8+ T cells (Wei et al, 2006). In psoriasis, the two most important effects of IL-20 are the inhibition of normal terminal differentiation of keratinocytes and the induction of anti-bacterial proteins (Wolk et al, 2009a).…”