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TLR7 promotes skin inflammation via activating NFκB-mTORC1 axis in rosacea

Yaqun Huang1,2,3, Da Liu1,2,3, Mengting Chen1,2,3

  • 1Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.

Peerj
|October 2, 2023
PubMed

Insights

Toll-like receptor 7 (TLR7) plays a key role in rosacea inflammation. Targeting TLR7 may offer a new treatment for this chronic skin condition.

Area of Science:

  • Dermatology
  • Immunology
  • Molecular Biology

Background:

  • Rosacea is a chronic inflammatory skin condition linked to skin barrier defects and immune system imbalances.
  • The precise role of Toll-like receptors (TLRs) in rosacea pathogenesis remains unclear.

Purpose of the Study:

  • To investigate the involvement of TLRs, particularly TLR7, in the inflammatory processes of rosacea.
  • To elucidate the molecular mechanisms underlying TLR7's contribution to rosacea development.

Main Methods:

  • RNA-sequencing analysis of rosacea skin lesions.
  • LL37-induced rosacea-like mouse models.
  • Gene silencing and overexpression techniques in keratinocytes.
  • Analysis of signaling pathways including NFκB and mTORC1.

Main Results:

  • The TLR signaling pathway was significantly enriched in rosacea skin lesions, with TLR7 showing a positive correlation with disease severity.
  • Silencing TLR7 in a mouse model inhibited the development of rosacea-like skin inflammation.
  • Overexpression of TLR7 in keratinocytes activated the NFκB and mTORC1 pathways.
  • The TLR7/NFκB/mTORC1 axis promoted cytokine/chemokine production and CD4+ T cell migration to lesional skin.

Conclusions:

  • TLR7 is a critical factor in rosacea pathogenesis.
  • The TLR7/NFκB/mTORC1 signaling axis is a key driver of inflammation in rosacea.
  • TLR7 represents a potential therapeutic target for rosacea treatment.
Keywords:
MTORNFκBRosaceaSkin immunologySkin inflammationTLR7

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