Interleukin (IL)-17 versus IL-27: opposite effects on tumor necrosis factor-α-mediated chemokine production in human keratinocytes.

Abstract

Tumor necrosis factor (TNF)-α is known to play a pivotal role in the pathogenesis of psoriasis. TNF-α has been shown to act directly on keratinocytes, thereby inducing the production of various kinds of chemokines, which contributes to the infiltration of leucocytes into the psoriatic lesions. Recent studies have shown that both interleukin (IL)-17 and IL-27 are increased in psoriatic lesional tissue. However, the interactions between TNF-α, IL-17 and IL-27 in chemokine production by keratinocytes have not been fully elucidated. Here, we examined in human keratinocytes how TNF-α, IL-17 and IL-27 affect production of chemokines that are involved in the pathogenesis of psoriasis. We found that IL-17 and IL-27 exert opposite effects on TNF-α-mediated chemokine production. This suggests that lesional balance of IL-17 and IL-27 is involved in the recruitment of T cells, natural killer cells, neutrophils, monocytes or dendritic cells, thereby affecting inflammation in skin diseases.

• Authors: Susumu Fujiwara, Hiroshi Nagai, Shuntaro Oniki, Takayuki Yoshimoto, Chikako Nishigori
• Journal: Experimental dermatology (Exp Dermatol) Vol. 21 Issue 1 Pg. 70-2 (Jan 2012) ISSN: 1600-0625 [Electronic] Denmark
• PMID: 22082171 (Publication Type: Letter, Research Support, Non-U.S. Gov't)
• Copyright: © 2011 John Wiley & Sons A/S.

Chemical References

• Chemokines
• Interleukin-17
• Interleukins
• MYDGF protein, human
• Tumor Necrosis Factor-alpha

Topics

• Chemokines (metabolism)
• Humans
• Interleukin-17 (metabolism)
• Interleukins (metabolism)
• Keratinocytes (metabolism)
• Psoriasis (etiology)
• Tumor Necrosis Factor-alpha (metabolism)