Antimicrobial peptide induction pathways in keratinocytes and epithelial cells

Antimicrobial peptide (AMP) induction pathways in keratinocytes and epithelial cells are essential components of the innate immune barrier, providing rapid defense against pathogens and contributing to tissue repair. These pathways are activated by a variety of stimuli, including pathogen-associated molecular patterns (PAMPs) via Toll-like receptors (TLRs), and endogenous ligands like 1,25-dihydroxyvitamin D3 via the Vitamin D Receptor (VDR) (Gombart et al., 2005; Wang et al., 2004). Key signaling mediators include the JAK-STAT pathway (activated by IL-17 and IL-22) and the NF-κB pathway, which drive the expression of major AMPs such as cathelicidin (LL-37), human beta-defensins (hBD-2, hBD-3), and S100 proteins (Liang et al., 2006; Wolk et al., 2004). In clinical practice, these pathways are targeted to treat inflammatory skin diseases; for example, VDR agonists are used to boost AMP production and barrier function, while biologics targeting the IL-17/IL-23 axis are used to suppress the pathological over-induction of AMPs and associated inflammation in psoriasis (Nomura et al., 2003; Mempel et al., 2003). Understanding the balance of these pathways is crucial, as insufficient AMP levels predispose patients to recurrent infections (e.g., in atopic dermatitis), while excessive levels can drive auto-inflammatory loops.

Other names

AMP induction signalingEpithelial innate immune pathwaysKeratinocyte antimicrobial response

Modulation of AMP expression through the activation of nuclear receptors (VDR) or the inhibition of pro-inflammatory cytokine signaling (IL-17/IL-22) that drives AMP transcription.