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VCAM-1 blockade delays disease onset, reduces disease severity and inflammatory cells in an atopic dermatitis model

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Title: VCAM-1 blockade delays disease onset, reduces disease severity and inflammatory cells in an atopic dermatitis model
Author(s): Chen, Lin; Lin, Shao-xia; Amin, Sanober; Overbergh, Lut; Maggiolino, Giacomo; Chan, Lawrence
Subject(s): atopic dermatitis inflammation ICAM-1 VCAM-1
Abstract: We investigated the roles of critical adhesion molecules ICAM-1 and VCAM-1 in a keratin-14 IL-4 transgenic (Tg) mouse model of atopic dermatitis, the skin lesions of which are characterized by prominent inflammatory cell infiltration, significantly increased mRNAs and proteins of ICAM-1, VCAM-1, E-selectin, P-selectin, L-selectin, and PSGL-1, and significantly increased numbers of dermal vessels expressing these adhesion molecules. We tested the hypotheses that deletion or blockade of these molecules may impede the inflammation by examining the disease progresses in the Tg mice crossed with ICAM-1 knockout mice and Tg mice received anti-VCAM-1 neutralizing antibody. While the findings of the ICAM-1-knockout Tg mice (Tg/ICAM-1-/-) developed skin lesions similar to wide type ICAM-1 Tg mice (Tg/ICAM-1+/+) were surprising, a compensatory mechanism may account for it: the frequency of VCAM-1 ligand, CD49d, on CD3+ T cells in the lesional skin significantly increased in the Tg/ICAM-1-/- mouse, compared to the Tg/ICAM-1+/+ mice. By contrast anti-VCAM-1-treated Tg/ICAM-1-/- or Tg/ICAM-1+/+ mice had significantly delayed onset of skin inflammation compared to isotype antibody-treated groups. Moreover, anti-VCAM-1 significantly reduced the skin inflammation severity in Tg/ICAM-1+/+ mice, accompanied with reduction of mast cell, eosinophil, and CD3+ T-cell infiltration. VCAM-1 is more critical in developing skin inflammation in this model.
Issue Date: 2010-01-12
Publisher: Nature Publishing Group
Citation Info: Chen, L., Lin, S. X., Amin, S., Overbergh, L., Maggiolino, G., & Chan, L. S. 2010. VCAM-1 blockade delays disease onset, reduces disease severity and inflammatory cells in an atopic dermatitis model. Immunology and Cell Biology., 88(3): 334-342. DOI: 10.1038/icb.2009.107
Type: Article
Description: Post print version of article may differ from published version. The definitive version is available through Nature Publishing Group at DOI: 10.1038/icb.2009.107
URI: http://hdl.handle.net/10027/7349
ISSN: 1440-1711
Date Available in INDIGO: 2011-03-01
 

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