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Cited by 354

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

β-Defensin-2 Expression Is Regulated by TLR Signaling in Intestinal Epithelial Cells

Vora, Puja, Youdim, Adrienne, Thomas, Lisa S, Fukata, Masayuki, Tesfay, Samuel Y, Lukasek, Katie, Michelsen, Kathrin S, Wada, Akihiro, Hirayama, Toshiya, Arditi, Moshe, Abreu, Maria T·2004·The Journal of Immunology

Abstract

The intestinal epithelium serves as a barrier to the intestinal flora. In response to pathogens, intestinal epithelial cells (IEC) secrete proinflammatory cytokines. To aid in defense against bacteria, IEC also secrete antimicrobial peptides, termed defensins. The aim of our studies was to understand the role of TLR signaling in regulation of β-defensin expression by IEC. The effect of LPS and peptidoglycan on β-defensin-2 expression was examined in IEC lines constitutively or transgenically expressing TLRs. Regulation of β-defensin-2 was assessed using promoter-reporter constructs of the human β-defensin-2 gene. LPS and peptidoglycan stimulated β-defensin-2 promoter activation in a TLR4- and TLR2-dependent manner, respectively. A mutation in the NF-κB or AP-1 site within the β-defensin-2 promoter abrogated this response. In addition, inhibition of Jun kinase prevents up-regulation of β-defensin-2 protein expression in response to LPS. IEC respond to pathogen-associated molecular patterns with expression of the antimicrobial peptide β-defensin-2. This mechanism may protect the intestinal epithelium from pathogen invasion and from potential invaders among the commensal flora.

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Crossref · 10.4049/jimmunol.173.9.5398

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Metadata

Authors
Vora, P., Youdim, A., Thomas, L. S., Fukata, M., Tesfay, S. Y., Lukasek, K., Michelsen, K. S., Wada, A., Hirayama, T., Arditi, M., & Abreu, M. T.
Venue
The Journal of Immunology
Published
2004-11-01
Volume
173
Issue
9
Pages
5398-5405
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
OpenAlex
W2115360262
Cited by
354
References
4
FWCI
26.01
Type
journal article
Language
en
Open access
closed

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