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Zhang X.,Helmholtz Center Berlin | Sun G.,Leibniz Institute for Analytical Sciences | Hovestadt M.,Institute For Medizinische Immunologie | Syritski V.,Tallinn University of Technology | And 5 more authors.
Electrochemistry Communications

We have developed and investigated a new route to functionalise Au surfaces using maleimide groups. This functionalisation has been performed by grafting aminophenyl (AP) via an electrochemical reduction of 4-aminophenyldiazonium salt in acetonitrile solution and the subsequent chemical binding of N-(2-carboxyethyl) maleimide (NCEM). The resulting maleimide functionalised surface was interacted with a cysteine-modified peptide. The grafting of AP was monitored by the occurrence of NH2 and aryl ring vibrations, whereas the binding of the NCEM led to a strong and sharp peak because of the C O stretching mode. The immobilisation of the peptide was identified by the appearance of the amide I band. Half of the maleimide surface groups reacted with the peptide because of steric hindrance. The charge efficiency for the AP layer formation was about 45% at a thickness of about 6-8 nm. © 2010 Elsevier B.V. Source

Witte E.,Institute For Medizinische Immunologie | Witte K.,Institute For Medizinische Immunologie | Sabat R.,Institute For Medizinische Immunologie | Sabat R.,Charite - Medical University of Berlin | And 2 more authors.

Interleukin (IL)-22 and IL-20 are two cytokines of the IL-10 family that are of great importance for the skin biology. Whereas IL-22 is produced by activated T cells (T1, T22, T17) and NK cells, the cellular sources of IL-20 include monocytes, dendritic cells and keratinocytes. Both cytokines act via similar receptors, which in the skin are especially present on keratinocytes, but do not influence cells of the immune system. In psoriasis IL-22 and IL-20 are massively present in the skin as well as in the blood. The current research findings allow to hypothesize, that IL-22 and IL-20 are directly causing the clinically visible epidermal alterations in psoriasis. In fact, the regulation of keratinocyte functions by IL-22 and IL-20 in vitro and in vivo mirrors the pathologic keratinocyte alterations in psoriasis. In vitro both cytokines reduce the terminal differentiation and simultaneously increase the innate immunity of the keratinocytes. Additionally, they increase the mobility and the production of neutrophilic granulocyte attracting chemokines in these cells. Mice with genetic modifications causing constitutively high systemic levels of IL-22 or IL-20 have a psoriasis-like skin phenotype with acanthosis, hypogranularity and hyperkeratosis. In contrast, blocking these cytokines prevents the pathological skin alterations in different murine psoriasis-models. A therapeutic strategy directed against IL-22 and IL-20 would therefore be an innovative approach for treating this disorder interfering with the final phase of the psoriasis pathogenesis. By the selective action of IL-22 and IL-20 on keratinocytes without influencing immune cells such a therapy would be expected to be not accompanied by severe side effects. Source

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