Beta-defensins are a family of small cationic antimicrobial peptides (36-45 amino acids, MW ~4-5 kDa) produced by epithelial cells throughout the body. The three best-characterized human beta-defensins are HBD-1 (constitutive), HBD-2 (inducible by infection/inflammation), and HBD-3 (broad-spectrum, including anti-MRSA activity). They are key components of innate mucosal immunity and serve as endogenous reference molecules rather than therapeutic products.
Category: Antimicrobial / Immune. Evidence rating: D (animal/preclinical only).
Clinical status: Endogenous peptides. No therapeutic product in clinical development. Studied as biomarkers and templates for antimicrobial drug design.
Beta-defensins are cationic amphipathic peptides containing three conserved disulfide bonds in a characteristic beta-sheet structure. They kill microorganisms primarily through electrostatic interaction with negatively charged microbial membranes, causing membrane disruption and cell lysis. HBD-1…
Safety considerations: Endogenous peptides naturally present in human tissues; Overexpression is associated with chronic inflammatory conditions (psoriasis, IBD); No exogenous therapeutic formulations exist for safety assessment.
Reviewed by the PeptideAtlas Editorial Team. Last reviewed: 2026-08-12.
Related peptides: LL-37, Alpha-Defensins, Lactoferricin.
Compare: Beta-Defensins vs LL-37, Beta-Defensins vs Alpha-Defensins, Beta-Defensins vs Lactoferricin.
No. Beta-defensins are endogenous peptides produced by your own epithelial cells. They are not available as supplements or therapeutic products. Research focuses on understanding their biology and using them as templates for new antimicrobial drugs.
Alpha-defensins (HNP-1 through 4, HD-5, HD-6) are primarily produced by neutrophils and Paneth cells, while beta-defensins (HBD-1, 2, 3) are produced by epithelial cells. They differ in disulfide bond connectivity and tissue distribution but share broadly similar antimicrobial mechanisms.
Beta-defensins are a major component of skin innate immunity. Psoriatic skin overexpresses HBD-2 and HBD-3, which may explain resistance to skin infections in psoriasis. Conversely, atopic dermatitis skin has reduced beta-defensin expression, contributing to increased susceptibility to S. aureus and herpes simplex virus infections.