title: Important roles of platelets as immune cells in the skin.
abstract: Platelets work as immune cells by initiating and modulating inflammatory and immune responses, in addition to having prominent functions in hemostasis and thrombosis. They store a multitude of immune-associated molecules in their granules. Upon activation in response to various factors such as thrombin, chemokines, and microbial toxins, platelets express adhesive and immune receptors such as P-selectin, CD40 ligand, and Toll-like receptors on their surface, and release soluble mediators such as chemokines, cytokines, and antimicrobial peptides. In this way, platelets interact with endothelial cells and leukocytes including dendritic cells, T cells, B cells, neutrophils, monocytes, and natural killer cells, both directly by cell to cell contact and indirectly via secretion of soluble mediators. In cutaneous inflammatory diseases such as atopic dermatitis and psoriasis, platelets circulate in an activated state, and the degree of platelet activation correlates with disease severity. Platelets are closely linked to the pathogenesis of inflammatory skin diseases, including atopic dermatitis, contact dermatitis, and psoriasis, via several pathomechanisms, e.g. increasing leukocyte rolling on the endothelium via formation of platelet-leukocyte complexes, recruiting leukocytes into inflamed skin via release of inflammatory mediators including chemokines, inhibiting monocytic apoptosis, inducing neutrophil phagocytosis, promoting allergic sensitization, provoking pruritus, and regulating inflammation. Platelets can also recognize bacterial pathogens through interactions via Toll-like receptors, leading to subsequent elimination of the bacteria by release of antimicrobial peptides or by aggregation of platelets around the bacteria. Thus, platelets are deeply involved in the innate and acquired immune responses in the skin via interactions with leukocytes and the endothelium.
authors.affiliation: Department of Dermatology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, 465, Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, Japan. Electronic address: risat@koto.kpu-m.ac.jp.
authors.forename: Risa
authors.initials: R
authors.lastname: Tamagawa-Mineoka
mesh_terms: D000917:Antibody Formation; D001792:Blood Platelets / Q000276:immunology*; D003872:Dermatitis / Q000276:immunology*; D003876:Dermatitis, Atopic / Q000276:immunology; D003877:Dermatitis, Contact / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D007249:Inflammation / Q000276:immunology; D007962:Leukocytes / Q000276:immunology; D011565:Psoriasis / Q000276:immunology
keywords: Atopic dermatitis; Contact dermatitis; Infection; Inflammation; Platelet; Psoriasis