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dc.contributor.authorAbrams, Judith R.en_US
dc.contributor.authorLebwohl. Mark G.en_US
dc.contributor.authorGuzzo, Cynthia A.en_US
dc.contributor.authorJegasothy. Brian V.en_US
dc.contributor.authorGoldfarb, Michael T.en_US
dc.contributor.authorGoffe, Bernard S.en_US
dc.contributor.authorMenter, Alanen_US
dc.contributor.authorLowe, Nicholas J.en_US
dc.contributor.authorKrueger, Geralden_US
dc.contributor.authorBrown, Michael J.en_US
dc.contributor.authorWeiner, Russell S.en_US
dc.contributor.authorBirkhofer, Martin J.en_US
dc.contributor.authorWarner, Garvin L.en_US
dc.contributor.authorBerry, Karen K.en_US
dc.contributor.authorLinsley, Peter S.en_US
dc.contributor.authorKrueger, James G.en_US
dc.contributor.authorOchs, Hans D.en_US
dc.contributor.authorKelley, Susan L.en_US
dc.contributor.authorKang, Sewonen_US
dc.date.accessioned2009-12-15T21:09:47Z
dc.date.available2009-12-15T21:09:47Z
dc.date.issued1999en_US
dc.identifier.citationAbrams JR, Lebwohl MG, Guzzo CA, et al. CTLA4Ig-mediated blockade of T-cell costimulation in patients with psoriasis vulgaris. J Clin Invest. 1999;103(9):1243-1252.en_US
dc.identifier.other10.1172/JCI5857en_US
dc.identifier.urihttp://www.jci.org/articles/view/5857en_US
dc.identifier.urihttp://hdl.handle.net/1773/15538
dc.description.abstractEngagement of the B7 family of molecules on antigen-presenting cells with their T cell–associated ligands, CD28 and CD152 (cytotoxic T lymphocyte–associated antigen-4 [CTLA-4]), provides a pivotal costimulatory signal in T-cell activation. We investigated the role of the CD28/CD152 pathway in psoriasis in a 26-week, phase I, open-label dose-escalation study. The importance of this pathway in the generation of humoral immune responses to T cell–dependent neoantigens, bacteriophage φX174 and keyhole limpet hemocyanin, was also evaluated. Forty-three patients with stable psoriasis vulgaris received 4 infusions of the soluble chimeric protein CTLA4Ig (BMS-188667). Forty-six percent of all study patients achieved a 50% or greater sustained improvement in clinical disease activity, with progressively greater effects observed in the highest-dosing cohorts. Improvement in these patients was associated with quantitative reduction in epidermal hyperplasia, which correlated with quantitative reduction in skin-infiltrating T cells. No markedly increased rate of intralesional T-cell apoptosis was identified, suggesting that the decreased number of lesional T cells was probably likely attributable to an inhibition of T-cell proliferation, T-cell recruitment, and/or apoptosis of antigen-specific T cells at extralesional sites. Altered antibody responses to T cell–dependent neoantigens were observed, but immunologic tolerance to these antigens was not demonstrated. This study illustrates the importance of the CD28/CD152 pathway in the pathogenesis of psoriasis and suggests a potential therapeutic use for this novel immunomodulatory approach in an array of T cell–mediated diseases.en_US
dc.language.isoen_USen_US
dc.titleCTLA4Ig-mediated blockade of T-cell costimulation in patients with psoriasis vulgarisen_US
dc.typeArticleen_US


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