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Inhibition of Cutaneous UV Light–induced Tumor Necrosis Factor‐α Protein Production by Allotrap 1258, a Novel Immunomodulatory Peptide ¶
Author(s) -
Oberyszyn Tatiana M.,
Robertson Fredika M.,
Tober Kathleen L.,
Ross Mary S.,
Parrett Michelle L.,
Wilgus Traci A.,
Iyer Suhasini,
Woo Jacky,
Buelow Roland
Publication year - 2001
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1562/0031-8655(2001)0730184ioculi2.0.co2
Subject(s) - hairless , in vivo , tumor necrosis factor alpha , peptide , immune system , pharmacology , in vitro , epidermis (zoology) , inflammation , chemistry , cancer research , immunology , biology , biochemistry , microbiology and biotechnology , anatomy
ABSTRACT Peptides derived from the heavy chain of the HLA Class‐I molecules have been shown to modulate immune responses both in vivo and in vitro. Using a computer‐aided rational drug design approach, novel immunomodulatory peptides were designed based on peptide 2702.75–85, derived from HLA‐B2702. Several peptides were identified which had increased immunomodulatory activity, including peptides RDP1258 and its d ‐isomer the peptide Allotrap 1258. The present study using Skh/hr hairless mouse skin model evaluated the in vivo effects of Allotrap 1258 on acute UVB‐induced skin inflammation. Here we demonstrate that intraperitoneal administration of Allotrap 1258 1 h prior to UV exposure resulted in significantly diminished levels of UV‐induced tumor necrosis factor (TNF)‐α protein production in the epidermis but had no effect on other parameters of the acute UV‐induced inflammatory response. By virtue of its ability to suppress TNF‐α protein production, Allotrap 1258 could prove to be an effective modulator of inflammatory responses.