# Nucleic acid-induced chemokine expression in keratinocytes: Implications for skin inflammation

## TL;DR

This study explores how nucleic acids affect chemokine expression in skin cells, which could help understand chronic skin inflammation.

## Contribution

The study identifies nucleic acids as inducers of specific chemokines in keratinocytes and highlights unknown pattern recognition receptors involved.

## Key findings

- Cytoplasmic nucleic acids strongly induce CCL2, CXCL10, and CX3CL1 mRNA in keratinocytes via NF-κB activation.
- Alternative splicing of chemokines in keratinocytes was not detected.
- The specific pattern recognition receptors responsible for the observed activation remain unidentified.

## Abstract

Chemokines play an important role in the pathogenesis of skin diseases, such as psoriasis, atopic dermatitis, vitiligo, and alopecia areata. Recently literature data supports the theory that alternatively spliced isoforms of these molecules may serve as potential regulators in these diseases. Since self-derived nucleic acids are main culprits in chronic skin diseases we compared the effects of synthetic RNA- and DNA-induced inflammation on the expression levels of chemokines in human keratinocytes. We found that cytoplasmic nucleic acids are potent inducers of monocyte chemoattractant protein-1 (CCL2), interferon gamma inducible protein-10 (CXCL10) and fractalkine (CX3CL1) mRNA-expression, mainly through NF-κB activation, but the pattern recognition receptors responsible for inducing this activation are still unknown. Alternative splicing of these chemokines in keratinocytes was not detected, suggesting other regulatory mechanisms for chemokine activity.