International Immunology Advance Access originally published online on October 13, 2006
International Immunology 2006 18(12):1729-1736; doi:10.1093/intimm/dxl107
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The anti-microbial peptide LL-37 inhibits the activation of dendritic cells by TLR ligands
1 Department of Internal Medicine, Division for Pulmonary Diseases, Baldingerstrasse 1, 35043 Marburg, Germany
2 Department of Microbiology, Hospital of the University of Marburg, Philipps-Universtät Marburg, Baldingerstrasse 1, 35043 Marburg, Germany
Correspondence to: R. Bals; E-mail: bals{at}mailer.uni-marburg.de
The endogenous anti-microbial peptide LL-37/hCAP-18 is an effector molecule of the innate host defense system at surfaces of the body. Besides its direct anti-microbial activity, the peptide interacts with different cell types. Dendritic cells (DCs) play a central role in mucosal host defense. It was the aim of the study to determine whether LL-37 modulates the response of DCs to pathogen-associated molecular patterns. Monocyte-derived DCs were stimulated with the Toll-like receptors (TLRs) ligands LPS, lipoteichoic acid and flagellin. We measured classical markers of DC maturation and assayed the ability of the DCs to activate T cell responses. Co-incubation with LL-37 resulted in suppressed activation of DCs. Levels of released IL-6, IL-12p70 and TNF-
and surface expression of HLA-DR, CD80, CD83, CD86 and the chemokine receptor CCR7 were decreased. Exposure of DCs to LL-37 during LPS exposure induced co-cultured naive T cells to produce less IL-2 and IFN-
and decreased their proliferation. The response of memory T cells to a recall antigen was also decreased. In conclusion, we demonstrate that the anti-microbial peptide LL-37 inhibits the activation of DCs by TLR ligands. We propose that LL-37 is a regulator of host defense responses at the intersection of innate and adaptive immune systems.
Keywords: cathelicidin, innate immunity, regulation, Toll-like receptor
Transmitting editor: L. Moretta
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