1. Antimicrobial peptides and the skin immune defense system
Jürgen Schauber, MD, Richard L. Gallo, MD, PhD 
Journal of Allergy and Clinical Immunology 
Volume 122, Issue 2, Pages (August 2008)
DOI: /j.jaci
Copyright © 2008 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2. Fig 1
Models for cell activation by cathelicidins. Multiple mechanisms have been proposed for cathelicidins to stimulate a cellular response. Responses are dependent on activation of G protein–coupled receptors and transactivation of the epidermal growth factor receptor or secondary to intracellular Ca2+ mobilization or a change in cell membrane function, leading to alterations in receptor responses. Finally, cathelicidins can influence the function of TLRs through both direct and indirect pathways. EGF-R, Epidermal growth factor receptor; IP-10, IFN-γ–inducible protein 10; MCP-1, monocyte chemoattractant protein 1; MIP3α, macrophage inflammatory protein 3α; ERK, extracellular signal-regulated kinase; MAPK, mitogen-activated protein kinase; STAT, signal transducer and activator of transcription.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2008 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3. Fig 2
Mechanisms of vitamin D3 activation and cathelicidin response. Extrarenal metabolism of vitamin D3 by keratinocytes provides a system for rapid control of cathelicidin expression. Activation of 25D3 to 1,25D3 requires 2 hydroxylation steps that occur sequentially in the liver and kidney. However, keratinocytes also express CYP27B1, a 1α-hydroxylase that activates 1,25D3. CYP27B1 expression in keratinocytes is controlled by danger signals during skin infection and tissue damage.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2008 American Academy of Allergy, Asthma & Immunology Terms and Conditions