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Differential regulation of beta-defensin expression in human skin by microbial stimuli

Sørensen, Ole E LU ; Thapa, D R ; Rosenthal, A ; Liu, L D ; Roberts, A A and Ganz, T (2005) In Journal of Immunology 174(8). p.4870-4879
Abstract
In response to infection, epithelia mount an innate immune response that includes the production of antimicrobial peptides. However, the pathways that connect infection and inflammation with the induction of antimicrobial peptides in epithelia are not understood. We analyzed the molecular links between infection and the expression of three antimicrobial peptides of the beta-defensin family, human beta-defensin (hBD)-1, hBD-2, and hBD-3 in the human epidermis. After exposure to microbe-derived molecules, both monocytes and lymphocytes stimulated the epidermal expression of hBD-1, hBD-2, and hBD-3. The induced expression of hBD-3 was mediated by transactivation. of the epidermal growth factor receptor. The mechanisms of induction of hBD-1... (More)
In response to infection, epithelia mount an innate immune response that includes the production of antimicrobial peptides. However, the pathways that connect infection and inflammation with the induction of antimicrobial peptides in epithelia are not understood. We analyzed the molecular links between infection and the expression of three antimicrobial peptides of the beta-defensin family, human beta-defensin (hBD)-1, hBD-2, and hBD-3 in the human epidermis. After exposure to microbe-derived molecules, both monocytes and lymphocytes stimulated the epidermal expression of hBD-1, hBD-2, and hBD-3. The induced expression of hBD-3 was mediated by transactivation. of the epidermal growth factor receptor. The mechanisms of induction of hBD-1 and hBD-3 were distinct from each other and from the IL-1-dependent induction of hBD-2 expression. Thus during inflammation, epidermal expression of beta-defensins is mediated by at least three different mechanisms. (Less)
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author
; ; ; ; and
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Immunology
volume
174
issue
8
pages
4870 - 4879
publisher
American Association of Immunologists
external identifiers
  • wos:000228234600054
  • pmid:15814714
ISSN
1550-6606
language
English
LU publication?
no
id
90223c0d-c401-4225-a750-83add0aa8766 (old id 240110)
alternative location
http://www.jimmunol.org/cgi/content/abstract/174/8/4870
date added to LUP
2016-04-01 16:37:42
date last changed
2018-11-21 20:42:53
@article{90223c0d-c401-4225-a750-83add0aa8766,
  abstract     = {{In response to infection, epithelia mount an innate immune response that includes the production of antimicrobial peptides. However, the pathways that connect infection and inflammation with the induction of antimicrobial peptides in epithelia are not understood. We analyzed the molecular links between infection and the expression of three antimicrobial peptides of the beta-defensin family, human beta-defensin (hBD)-1, hBD-2, and hBD-3 in the human epidermis. After exposure to microbe-derived molecules, both monocytes and lymphocytes stimulated the epidermal expression of hBD-1, hBD-2, and hBD-3. The induced expression of hBD-3 was mediated by transactivation. of the epidermal growth factor receptor. The mechanisms of induction of hBD-1 and hBD-3 were distinct from each other and from the IL-1-dependent induction of hBD-2 expression. Thus during inflammation, epidermal expression of beta-defensins is mediated by at least three different mechanisms.}},
  author       = {{Sørensen, Ole E and Thapa, D R and Rosenthal, A and Liu, L D and Roberts, A A and Ganz, T}},
  issn         = {{1550-6606}},
  language     = {{eng}},
  number       = {{8}},
  pages        = {{4870--4879}},
  publisher    = {{American Association of Immunologists}},
  series       = {{Journal of Immunology}},
  title        = {{Differential regulation of beta-defensin expression in human skin by microbial stimuli}},
  url          = {{http://www.jimmunol.org/cgi/content/abstract/174/8/4870}},
  volume       = {{174}},
  year         = {{2005}},
}