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Multispecific myeloid defensins

Lehrer, Robert I

Current Opinion in Hematology: January 2007 - Volume 14 - Issue 1 - p 16–21
Myeloid biology

Purpose of review: This review describes recent progress in our understanding of defensins and their contributions to innate immunity. Defensins are small, cysteine-rich endogenous antibiotic peptides. Human neutrophils contain large amounts of three α-defensins (HNP-1–HNP-3), and smaller amounts of a fourth, HNP-4. Monocytes and macrophages generally lack defensins, but they release messengers that induce the synthesis of β-defensins in epithelial cells.

Recent findings: In addition to their antimicrobial and immunomodulatory effects, HNP-1–HNP-3 possess antiviral and toxin-neutralizing properties. Induction of β-defensins in epithelial cells is mediated by cell-surface Toll-like receptors or cytoplasmic peptidoglycan receptors that can recognize pathogen-associated molecules. Mutations in Nod2, a cytoplasmic peptidoglycan receptor, are associated with reduced levels of intestinal α-defensins and ileal Crohn's disease. Human defensin genes show marked copy-number polymorphism. High level constitutive expression of defensins may afford protection against HIV-1 and other defensin-sensitive pathogens. Theta-defensins (cyclic octadecapeptides found in nonhuman primates) have impressive antiviral and antitoxic properties.

Summary: The multiple properties of defensins contribute to human innate immunity against bacteria, bacterial toxins, and viruses.

David Geffen School of Medicine at UCLA, Los Angeles, California, USA

Correspondence to Robert I. Lehrer, Professor of Medicine, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA Tel: +1 310 825 5340; Fax: +1 310 206 8766; e-mail: rlehrer@mednet.ucla.edu

Disclosures: The author affirms that any opinions expressed in this review are his own, that no conflict of interest exists, and that his own research has been funded exclusively by government grants for the past decade.

© 2007 Lippincott Williams & Wilkins, Inc.