Alefacept (anti-CD2) causes a selective reduction in circulating effector memory T cells (Tem) and relative preservation of central memory T cells (Tcm) in psoriasis

被引:62
作者
Chamian, Francesca [1 ]
Lin, Shao-Lee [1 ]
Lee, Edmund [1 ]
Kikuchi, Toyoko [1 ]
Gilleaudeau, Patricia [1 ]
Sullivan-Whalen, Mary [1 ]
Cardinale, Irma [1 ]
Khatcherian, Artemis [1 ]
Novitskaya, Inna [1 ]
Wittkowski, Knut M. [1 ]
Krueger, James G. [1 ]
Lowes, Michelle A. [1 ]
机构
[1] Rockefeller Univ, Invest Dermatol Lab, New York, NY 10021 USA
关键词
D O I
10.1186/1479-5876-5-27
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background: Alefacept (anti-CD2) biological therapy selectively targets effector memory T cells (Tem) in psoriasis vulgaris, a model Type 1 autoimmune disease. Methods: Circulating leukocytes were phenotyped in patients receiving alefacept for moderate to severe psoriasis. Results: In all patients, this treatment caused a preferential decrease in effector memory T cells (CCR7(-) CD45RA(-)) ( mean 63% reduction) for both CD4(+) and CD8(+) Tem, while central memory T cells (Tcm) ( CCR7(+) CD45RA(-)) were less affected, and nave T cells (CCR7(+) CD45RA(+)) were relatively spared. Circulating CD8(+) effector T cells and Type 1 T cells ( IFN-gamma- producing) were also significantly reduced. Conclusion: Alefacept causes a selective reduction in circulating effector memory T cells (Tem) and relative preservation of central memory T cells ( Tcm) in psoriasis.
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页数:7
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共 23 条
[1]   The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-γ, interleukin-2, and tumor necrosis factor-α, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations:: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients [J].
Austin, LM ;
Ozawa, M ;
Kikuchi, T ;
Walters, IB ;
Krueger, JG .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1999, 113 (05) :752-759
[2]  
BACCHMANN MF, 2003, J IMMUNOL, V190, P1383
[3]   Alefacept reduces infiltrating T cells, activated dendritic cells, and inflammatory genes in psoriasis vulgaris [J].
Chamian, F ;
Lowes, MA ;
Lin, SL ;
Lee, E ;
Kikuchi, T ;
Gilleaudeau, P ;
Sullivan-Whalen, M ;
Cardinale, I ;
Khatcherian, A ;
Novitskaya, I ;
Wittkowski, KM ;
Krueger, JG .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (06) :2075-2080
[4]   PROLONGATION OF ALLOGRAFT AND XENOGRAFT SURVIVAL IN MICE BY ANTI-CD2 MONOCLONAL-ANTIBODIES [J].
CHAVIN, KD ;
LAU, HT ;
BROMBERG, JS .
TRANSPLANTATION, 1992, 54 (02) :286-291
[5]  
Crawford K, 1999, J IMMUNOL, V163, P5920
[6]   Alefacept, an immunomodulatory recombinant FA-3/IgG1 fusion protein, induces CD16 signaling and CD2/CD16-dependent apoptosis of CD2+ cells [J].
da Silva, AJ ;
Brickelmaier, M ;
Majeau, GR ;
Li, ZF ;
Su, LH ;
Hsu, YM ;
Hochman, PS .
JOURNAL OF IMMUNOLOGY, 2002, 168 (09) :4462-4471
[7]  
Di Pucchio T, 2003, EUR J IMMUNOL, V33, P358
[8]  
Dumont C, 1998, J IMMUNOL, V160, P3797
[9]   ROLE OF LYMPHOCYTE ADHESION RECEPTORS IN TRANSIENT INTERACTIONS AND CELL LOCOMOTION [J].
DUSTIN, ML ;
SPRINGER, TA .
ANNUAL REVIEW OF IMMUNOLOGY, 1991, 9 :27-66
[10]   Treatment of chronic plaque psoriasis by selective targeting of memory effector T lymphocytes [J].
Ellis, CN ;
Krueger, GG .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 345 (04) :248-255