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* Laboratory of Molecular Immunoregulation, Division of Basic Sciences,
Intramural Research Support Program, SAIC Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland
Correspondence: Dr. Joost J. Oppenheim, LMI, DBS, NCI-FCRDC, Building 560, Room 21-89, Frederick, MD 21702-1201. E-mail: oppenhei{at}mail.ncifcrf.gov
Defensins, a family of cationic, structurally related, antimicrobial
peptides, contribute to host defense by disrupting the cytoplasmic
membrane of microbes. Here we show that human neutrophil defensins
selectively induce the migration of human
CD4+/CD45RA+ naive and CD8+, but
not CD4+/CD45RO+ memory, T cells. Moreover,
human neutrophil defensins are chemotactic for immature human dendritic
cells derived from either CD34+ progenitors or peripheral
blood monocytes. Upon maturation induced by treatment with tumor
necrosis factor 
(TNF-), dendritic cells lose their
responsiveness to human neutrophil defensins. The chemotactic effect of
human neutrophil defensins on both T and dendritic cells is pertussis
toxin-sensitive, suggesting that a Gi protein-coupled
receptor is responsible. Human neutrophil defensins are also
chemotactic for immature murine dendritic cells. These data suggest
that, in addition to their antimicrobial role, human neutrophil
defensins also contribute to adaptive immunity by mobilizing T cells
and dendritic cells.
Key Words: -defensins • chemotaxis • T lymphocytes
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