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Demodex TLR2 Expression in Sebocytes

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bjd16540-fig-0004-m.jpg
Image courtesy of Wily Online Library

A paper by Frank Powell, MD, The Charles Institute of Dermatology, University College Dublin, Belfield, Dublin 4, Ireland, and three other authors*, Demodex mites modulate sebocyte immune reaction: possible role in the pathogenesis of rosacea, concludes, “Our results also show for the first time that Demodex mites secrete bioactive molecules that reduced TLR2 expression in sebocytes.” 

So let’s break this down since this is demodectic rosacea news and you want to understand what all this means for those who want to dive deeper into rosacea investigative research.

First off, what are sebocytes? 
Answer
Any of the cells that make up the sebaceous glands, and secrete sebum. Wiktionary

What is TLR2?
Answer
One of a class of proteins that are single, membrane-spanning, non-catalytic receptors that identify structurally preserved molecules acquired from microbes known as Toll-Like Receptor 2 that play a key role in the innate immune system.

What does this mean?
If you look at the image above which shows on the left normal skin and how only a normal amount of demodex are able to regulate a TLR2 response so that the innate immune system doesn’t go into overdrive and respond to the demodex. For some unknown reason, in the image on the right with rosacea, when the demodex are increased the demodex can’t regulate the TLR2 response which initiates a cascade of molecular innate immune system activity. 

Why do the mites increase?
This has been one of the long time questions that the jury is still out on. More information

Conclusion
The paper written by Lacey, et. al, about understanding this activity of the mites regulating a TLR2 response at the molecular level may help in treating rosacea and understanding that demodex may be the cause of the innate immune system response. 

* British Journal of Dermatology
Demodex mites modulate sebocyte immune reaction: possible role in the pathogenesis of rosacea
N. Lacey, A. Russell‐Hallinan, C.C. Zouboulis, F.C. Powell

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