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Inhibitory Effects of CD99-derived Peptide CD99CRIII3 on the Extravasation of Monocytes and Inflammatory Reactions in Contact Dermatitis Mouse Model / 체질인류학회지
Korean Journal of Physical Anthropology ; : 143-149, 2018.
Artículo en Inglés | WPRIM | ID: wpr-718961
ABSTRACT
Leucocyte extravasation has been known to play an important role in inflammatory reactions including contact dermatitis. Previous studies suggested that CD99 regulates β1 integrin activity and may be a novel therapeutic target molecule for inflammatory diseases. In this study, the effects of CD99-derived peptide, CD99CRIII3, on inflammatory reactions in contact dermatitis mouse model were investigated. CD99CRIII3 decreased β1-integrin activity in human monocytic U937 cells. CD99CRIII3 inhibited the adhesion of U937 monocytes to human umbilical vein endothelial cells and their extravasation through human umbilical vein endothelial cells. CD99CRIII3 reduced inflammation in the phorbol myristate acetate-induced contact dermatitis mice in a dose-dependent manner. These results indicate that CD99CRIII3 suppresses the extravasation of monocytes and inflammatory reactions in the animal model of the contact dermatitis, suggesting that CD99CRIII3 could be a new drug candidate against inflammatory skin diseases.
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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Enfermedades de la Piel / Monocitos / Ácido Mirístico / Células U937 / Modelos Animales / Dermatitis por Contacto / Células Endoteliales de la Vena Umbilical Humana / Inflamación Límite: Animales / Humanos Idioma: Inglés Revista: Korean Journal of Physical Anthropology Año: 2018 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Enfermedades de la Piel / Monocitos / Ácido Mirístico / Células U937 / Modelos Animales / Dermatitis por Contacto / Células Endoteliales de la Vena Umbilical Humana / Inflamación Límite: Animales / Humanos Idioma: Inglés Revista: Korean Journal of Physical Anthropology Año: 2018 Tipo del documento: Artículo