β-Defensins: Linking Innate and Adaptive Immunity Through Dendritic and T Cell CCR6

Author:

Yang D.1,Chertov O.2,Bykovskaia S. N.3,Chen Q.1,Buffo M. J.3,Shogan J.3,Anderson M.4,Schröder J. M.5,Wang J. M.1,Howard O. M. Z.2,Oppenheim J. J.1

Affiliation:

1. Laboratory of Molecular Immunoregulation, Division of Basic Sciences,

2. Intramural Research Support Program, SAIC Frederick, National Cancer Institute–Frederick Cancer Research and Development Center, Frederick, MD 21702–1201, USA.

3. Allegheny University of Health Sciences, Pittsburgh, PA 15212, USA.

4. Magainin Research Institute, 5110 Campus Drive, Plymouth Meeting, PA 19642, USA.

5. Department of Dermatology, Christian Albrechts University of Kiel, Schittenhelmstrasse 7, D-24105 Kiel, Germany.

Abstract

Defensins contribute to host defense by disrupting the cytoplasmic membrane of microorganisms. This report shows that human β-defensins are also chemotactic for immature dendritic cells and memory T cells. Human β-defensin was selectively chemotactic for cells stably transfected to express human CCR6, a chemokine receptor preferentially expressed by immature dendritic cells and memory T cells. The β-defensin–induced chemotaxis was sensitive to pertussis toxin and inhibited by antibodies to CCR6. The binding of iodinated LARC, the chemokine ligand for CCR6, to CCR6-transfected cells was competitively displaced by β-defensin. Thus, β-defensins may promote adaptive immune responses by recruiting dendritic and T cells to the site of microbial invasion through interaction with CCR6.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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