Injury is a major inducer of epidermal innate immune responses during wound healing.

[1]  J. Schröder,et al.  Rhamnolipid‐induced shedding of flagellin from Pseudomonas aeruginosa provokes hBD‐2 and IL‐8 response in human keratinocytes , 2009, Cellular microbiology.

[2]  M. Mildner,et al.  Flagellin is the principal inducer of the antimicrobial peptide S100A7c (psoriasin) in human epidermal keratinocytes exposed to Escherichia coli , 2008, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[3]  J. Schröder,et al.  Mouse Beta-Defensin-14, an Antimicrobial Ortholog of Human Beta-Defensin-3 , 2008, Antimicrobial Agents and Chemotherapy.

[4]  T. Hehlgans,et al.  Identification and Biological Characterization of Mouse β-Defensin 14, the Orthologue of Human β-Defensin 3* , 2008, Journal of Biological Chemistry.

[5]  T. Ruzicka,et al.  S100A15, an antimicrobial protein of the skin: regulation by E. coli through Toll-like receptor 4. , 2007, The Journal of investigative dermatology.

[6]  Kathleen C. Lee,et al.  S100A7 (Psoriasin)--mechanism of antibacterial action in wounds. , 2007, The Journal of investigative dermatology.

[7]  Y. Helfrich,et al.  Injury enhances TLR2 function and antimicrobial peptide expression through a vitamin D-dependent mechanism. , 2007, The Journal of clinical investigation.

[8]  M. Malmsten,et al.  The contact system—a novel branch of innate immunity generating antibacterial peptides , 2006, The EMBO journal.

[9]  A. Schmidtchen,et al.  Injury-induced innate immune response in human skin mediated by transactivation of the epidermal growth factor receptor. , 2006, The Journal of clinical investigation.

[10]  Paul Martin,et al.  Inflammatory cells during wound repair: the good, the bad and the ugly. , 2005, Trends in cell biology.

[11]  T. Ganz,et al.  TGF-α Regulates TLR Expression and Function on Epidermal Keratinocytes1 , 2005, The Journal of Immunology.

[12]  H. Törmä,et al.  Vitamin D induces the antimicrobial protein hCAP18 in human skin. , 2005, The Journal of investigative dermatology.

[13]  G. Girolomoni,et al.  ERK1/2 Regulates Epidermal Chemokine Expression and Skin Inflammation1 , 2005, The Journal of Immunology.

[14]  T. Ganz,et al.  Differential Regulation of β-Defensin Expression in Human Skin by Microbial Stimuli1 , 2005, The Journal of Immunology.

[15]  J. Schröder,et al.  Psoriatic scales: a promising source for the isolation of human skin‐derived antimicrobial proteins , 2005, Journal of leukocyte biology.

[16]  K. Sayama,et al.  All-Trans-Retinoic Acid Induces Interleukin-8 via the Nuclear Factor-κB and p38 Mitogen-Activated Protein Kinase Pathways in Normal Human Keratinocytes , 2004 .

[17]  R. Gallo,et al.  Postsecretory Processing Generates Multiple Cathelicidins for Enhanced Topical Antimicrobial Defense1 , 2004, The Journal of Immunology.

[18]  S. Werner,et al.  Regulation of wound healing by growth factors and cytokines. , 2003, Physiological reviews.

[19]  E. Bröcker,et al.  TRAIL-induced apoptosis and gene induction in HaCaT keratinocytes: differential contribution of TRAIL receptors 1 and 2. , 2003, The Journal of investigative dermatology.

[20]  T. Ganz,et al.  Wound Healing and Expression of Antimicrobial Peptides/Polypeptides in Human Keratinocytes, a Consequence of Common Growth Factors1 , 2003, The Journal of Immunology.

[21]  E. Rajnavölgyi,et al.  Expression and function of Toll-like receptors 2 and 4 in human keratinocytes. , 2003, International immunology.

[22]  T. Ganz,et al.  By IL-1 Signaling, Monocyte-Derived Cells Dramatically Enhance the Epidermal Antimicrobial Response to Lipopolysaccharide1 , 2003, The Journal of Immunology.

[23]  M. Selsted,et al.  Antimicrobial Peptides from Human Platelets , 2002, Infection and Immunity.

[24]  P. Matzinger The Danger Model: A Renewed Sense of Self , 2002, Science.

[25]  Christina H. Park,et al.  Human beta-defensin-2 production in keratinocytes is regulated by interleukin-1, bacteria, and the state of differentiation. , 2002, The Journal of investigative dermatology.

[26]  I. Thorey,et al.  The Ca2+-binding Proteins S100A8 and S100A9 Are Encoded by Novel Injury-regulated Genes* , 2001, The Journal of Biological Chemistry.

[27]  V. Nizet,et al.  Cutaneous injury induces the release of cathelicidin anti-microbial peptides active against group A Streptococcus. , 2001, The Journal of investigative dermatology.

[28]  M. Pfaffl,et al.  A new mathematical model for relative quantification in real-time RT-PCR. , 2001, Nucleic acids research.

[29]  O. Grenet,et al.  An intrinsic antibiotic mechanism in wounds and tissue-engineered skin. , 2001, The Journal of investigative dermatology.

[30]  Y. Matsuzawa,et al.  Ectodomain Shedding of Epidermal Growth Factor Receptor Ligands Is Required for Keratinocyte Migration in Cutaneous Wound Healing , 2000, The Journal of cell biology.

[31]  M. Sticherling,et al.  Bioactive interleukin-8 is expressed in wounds and enhances wound healing. , 2000, The Journal of surgical research.

[32]  M. Nybo,et al.  Reduced expression of C5a receptors on neutrophils from cord blood , 1998, Archives of disease in childhood. Fetal and neonatal edition.

[33]  J. Schalkwijk,et al.  Expression of SKALP/elafin during wound healing in human skin , 1996, Archives of Dermatological Research.

[34]  K. Matsushima,et al.  Production of interleukin-8 by human dermal fibroblasts and keratinocytes in response to interleukin-1 or tumour necrosis factor. , 1989, Immunology.

[35]  S. Zigmond,et al.  Effects of cytochalasin B on polymorphonuclear leucocyte locomotion, phagocytosis and glycolysis. , 1972, Experimental cell research.

[36]  J. Schröder,et al.  Antimicrobial psoriasin (S100A7) protects human skin from Escherichia coli infection , 2005, Nature Immunology.

[37]  Artur,et al.  Activation of the complement system generates antibacterial peptides , 2004 .

[38]  Y. Aragane,et al.  Transforming growth factor-alpha induces interleukin-6 in the human keratinocyte cell line HaCaT mainly by transcriptional activation. , 1996, The Journal of investigative dermatology.

[39]  C. Kiritsy,et al.  Role of growth factors in cutaneous wound healing: a review. , 1993, Critical reviews in oral biology and medicine : an official publication of the American Association of Oral Biologists.

[40]  A. Böyum,et al.  Isolation of mononuclear cells and granulocytes from human blood. Isolation of monuclear cells by one centrifugation, and of granulocytes by combining centrifugation and sedimentation at 1 g. , 1968, Scandinavian journal of clinical and laboratory investigation. Supplementum.