人类具有38β-defensin基因加9-10个伪原（HTHNC网站上提供的详细信息，http://www.genenames.org/genefamilies/defb）。许多β-防御素由最近重复的基因编码，产生相同的转录物。命名法令人困惑，目前正在过渡。在整个途径中使用UNIPROT推荐的名称。
许多β-防御素显示出与感染相关的表达（Sahl等，2005，Pazgier等，2006）。All so far characterized beta-defensins, i.e. beta-defensin 1 (hBD1), 4A (hBD2), 103 (hBD3), 104 (hBD4), 106 (hBD6), 118 (hBD18) and 128 (hBD28) have antimicrobial properties (Pazgier et al. 2006). For beta-defensins 4A, 103 and 118 (hBD2, 3, and 18) this has been shown to correlate with membrane permeabilization effects (Antcheva et al. 2004, Sahl et al. 2005, Yenugu et al. 2004). Electrostatic interaction and disruption of microbial membranes is widely believed to the primary mechanism of action for beta-defensins. Two models explain how membrane disruption takes place, the 'pore model' which postulates that beta-defensins form transmembrane pores in a similar manner to alpha-defensins, and the 'carpet model', which suggests that beta-defensins act as detergents. Beta-defensins contain 6 conserved cysteine residues that in beta-defensins 1, 4A and 103 (hBD1-3) are experimentally confirmed to be cross-linked 1-5, 2-4, 3-6. The canonical sequence for beta-defensins is x2-10Cx5-6(G/A)xCX3-4Cx9-13Cx4-7CCxn. Structurally they are similar to alpha-defensins but with much shorter pre-regions. Though dimerization of some beta-defensins has been reported this is not the case for all and it is unclear whether it is required for function. The majority of functional studies have focused on beta-defensin 103 (hBD3), which has the most significant antimicrobial activity at physiological salt concentrations (Harder et al. 2001). Beta-defensin 103 is highly cationic with a net charge of +11 e0. It exhibits broad-spectrum antimicrobial activity against gram-positive bacteria and some gram-negative bacteria (Harder et al. 2001), though some species are highly resistant (Sahly et al. 2003). Sensitivity correlates with lipid composition of the membrane, with more negatively-charged lipids correlating with larger beta-defensin 103-induced changes in membrane capacitance (Bohling et al. 2006). Though membrane disruption is widely believed to be the primary mechanism of action of beta-defensins they have other antimicrobial properties, such as inhibition of cell wall biosynthesis (Sass et al. 2010), and chemoattractant effects (Yang et al. 1999, Niyonsaba et al. 2002, 2004). The chemotactic activity of beta-defensins 1, 4A and 103 (hBD1-3) for memory T cells and immature DCs is mediated through binding to the chemokine receptor CCR6 and probably another unidentified Gi-coupled receptor (Yang et al. 1999, 2000).

像防御素一样，人类植物疗法素LL37肽富含带正电荷的残留物（Lehrer＆Ganz 2002）。
某些β-防御素的表达可以响应于各种信号，例如细菌，病原体相关分子模式（PAMPs）或促炎细胞因子（Ganz 2003，Yang等人2004）。与alpha-defensins一样，拷贝数变化已经报告了DEFB4，DEFB103和DEFB104，每个二倍体基因组具有2-12份的个体。相比之下，DEFB1不显示这种变化，但展示了许多SNP（Hollox等，2003，Linzmier＆Ganz 2005）。