Sesja plenarna III
Antimicrobial peptides in the pathogenesis of psoriasis and atopic dermatitis

The elimination of bacterial, viral and fungal infections of the skin depends on the activation of mechanisms of natural (inbred) immunity and, upon contact with microorganisms, the induction of an acquired humoral and/or cellular specific immune response. Mechanisms related to receptors on keratinocytes which underlie natural immunity of the skin (TLR, NOD receptors) initiate production of self-defence substances, mainly peptides showing antibacterial activity, i.e. cathelicidin, defensins, granulysin, sphingosine and dermcidin. Defective antibacterial immunity in patients with atopic dermatitis is related to: 1. damaged barrier of stratum corneum (genetic defect of filaggrin gene and ceramides), 2. abnormal TLR2, NOD 1-2, and C14 receptor function as well as decreased activity of cells playing a role in immune reactions (neutrophils, NK cells and Langerhans cells), and 3. reduced production of antimicrobial peptides by keratinocytes. These phenomena are not altered in psoriatic epidermis; on the contrary, some of these peptides are released in excess. Antimicrobial immunity is not defective in patients with psoriasis despite the number of bacteria on the skin surface being markedly higher, and the epidermal barrier is also damaged as the result of non-terminal keratosis (parakeratosis) of the stratum corneum.