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Journal of Immunology Research
Volume 2014 (2014), Article ID 628289, 10 pages
Review Article

The New Insight into the Role of Antimicrobial Proteins-Alarmins in the Immunopathogenesis of Psoriasis

1Department of Dermatology, Venereology and Allergology, Wroclaw Medical University, ul. Chalubinskiego 1, 50-368 Wroclaw, Poland
2Department of Dermatology and Allergology, Ludwig-Maximilian University, Thalkirchner Straße 48, 80539 Munich, Germany

Received 1 February 2014; Revised 11 April 2014; Accepted 12 April 2014; Published 8 May 2014

Academic Editor: April Armstrong

Copyright © 2014 A. Batycka-Baran et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The pathognesis of psoriasis still remains not fully elucidated. Recent advances favor the idea that interactions between innate and adaptive immune response drive inflammatory process in this disease. Innate antimicrobial peptides and proteins (AMPs) are diverse group of small molecules that provide the first line of defense against invading pathogens. In recent years, the novel functions of AMPs have been identified. There are three subclasses among AMPs that have gained the special interest as a potentially important player in the pathogenesis of psoriasis: cathelicidin, S100 proteins, and defensins. These AMPs have been shown to modulate and trigger host immune response in psoriasis acting as interplayer between innate and adaptive immune mechanisms. Overexpressed in psoriatic lesions, they prime immune cells for enhanced production of proinflammatory mediators and act as chemoattractant for leukocytes. Therefore, the novel term describing AMPs alarmins has been suggested. As multifunctional player in pathogenesis of psoriasis, AMPs may constitute potential target for therapeutic interventions. However, further investigations are required to establish the methods of downregulation of the aberrant proinflammatory functions of AMPs without increasing the risk of infections.