Control of cutaneous antimicrobial peptides by vitamin D3

Yvonne Dombrowski, Mark Peric, Sarah Koglin, Thomas Ruzicka, Jürgen Schauber

Research output: Contribution to journalArticlepeer-review

37 Citations (Scopus)


Constant exposure to a wide variety of microbial pathogens represents a major challenge for our skin. Antimicrobial peptides (AMPs) are mediators of cutaneous innate immunity and protect primarily against microbial infections. Cathelicidins were among the first AMPs identified in human skin and recent evidence suggests that they exert a dual role in innate immune defense: At first, due to their antimicrobial activity they kill pathogens directly. In addition, these peptides initiate a potent host response to infection resulting in cytokine release, inflammation and a cellular response. Disturbed cathelicidin expression and function was observed in several common inflammatory skin diseases, such as psoriasis where cathelicidin peptide converts inert self-DNA and self-RNA into an autoimmune stimulus. In atopic dermatitis decreased levels of cathelicidin facilitating microbial superinfections have been discussed. Furthermore, abnormally processed cathelicidin peptides induce inflammation and a vascular response in rosacea. Until recently, the molecular mechanisms underlying cathelicidin regulation were unknown. Recently, the vitamin D3 pathway was identified as the major regulator of cathelicidin expression. Consequently, vitamin D3 entered the spotlight as an immune modulator with impact on both innate and adaptive immunity. Therapies targeting vitamin D3 signaling may provide new approaches for infectious and inflammatory skin diseases by affecting both innate and adaptive immune functions.
Original languageEnglish
Pages (from-to)401-8
Number of pages8
JournalArchives of Dermatological Research
Issue number6
Publication statusPublished - Aug 2010


  • Antigen Presentation
  • Autoimmune Diseases
  • Bacterial Infections
  • Blood Bactericidal Activity
  • Cathelicidins
  • Cholecalciferol
  • Gene Expression Regulation
  • Humans
  • Immunomodulation
  • Inflammation
  • Signal Transduction
  • Skin


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