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Development of an Economical DNA Delivery System by "Acufection" and its Application to Skin Research

Development of an Economical DNA Delivery System by "Acufection" and its Application to Skin Research

Published on: April 19, 2017

IL-18 and skin inflammation.

Miriam Wittmann¹, Andrew Macdonald, Julius Renne

¹Institute of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK. M.Wittmann@leeds.ac.uk

Autoimmunity Reviews

|March 17, 2009

Summary

This summary is machine-generated.

Interleukin-18 (IL-18) is crucial in skin inflammation, particularly Cutaneous Lupus Erythematosus (CLE). This cytokine drives TNFalpha release, leading to keratinocyte apoptosis, suggesting new therapeutic targets beyond anti-TNFalpha treatments.

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Development of an Economical DNA Delivery System by "Acufection" and its Application to Skin Research

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Published on: April 19, 2017

Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture

Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture

Published on: April 8, 2016

Area of Science:

Immunology
Dermatology
Molecular Biology

Background:

Interleukin-18 (IL-18) is a cytokine in the IL-1 family, involved in inflammasome activation.
Its role in chronic inflammatory diseases, including skin, gut, and kidney conditions, is increasingly recognized.
IL-18 is implicated in autoimmune responses and pathogen defense.

Purpose of the Study:

To summarize current knowledge on IL-18's role in human skin inflammation.
To focus on the specific involvement of IL-18 in Cutaneous Lupus Erythematosus (CLE).
To explore potential therapeutic strategies targeting IL-18 in skin inflammation.

Main Methods:

Review of existing literature on IL-18 and skin inflammation.
Analysis of IL-18's function in keratinocytes, particularly in the context of CLE.
In vitro studies examining the effects of IL-18 and TNFalpha on keratinocyte apoptosis.

Main Results:

IL-18 plays a significant role in CLE, acting upstream of TNFalpha.
IL-18 strongly induces TNFalpha release in CLE keratinocytes, but not in normal keratinocytes.
This TNFalpha induction leads to keratinocyte apoptosis, which can be blocked by TNFalpha inhibition in vitro.

Conclusions:

IL-18 is a key mediator in Cutaneous Lupus Erythematosus pathogenesis.
While anti-TNFalpha therapy shows efficacy in vitro, it's not suitable for lupus erythematosus (LE) conditions.
Targeting IL-18 presents a potential therapeutic avenue for managing skin inflammation in CLE.