Endogenous IL-8 acts as a CD16 co-activator for natural killer-mediated anti-CD20 B cell depletion in chronic lymphocytic leukemia

被引：18
作者：
Laprevotte, Emilie [1 ,2 ,3 ]
Ysebaert, Loic [1 ,2 ,3 ,4 ]
Klein, Christian
Valleron, Wilfried [1 ,2 ,3 ]
Blanc, Amandine [1 ,2 ,3 ]
Gross, Emilie [1 ,2 ,3 ]
Laurent, Guy [1 ,2 ,3 ,4 ]
Fournie, Jean-Jacques [1 ,2 ,3 ]
Quillet-Mary, Anne [1 ,2 ,3 ]
机构：
[1] Canc Res Ctr Toulouse, INSERM, UMR1037, Toulouse, France
[2] CNRS, ERL 5294, F-75700 Paris, France
[3] Univ Toulouse 3, F-31062 Toulouse, France
[4] CHU Purpan, Serv Hematol, Toulouse, France
来源：
LEUKEMIA RESEARCH | 2013年 / 37卷 / 04期
关键词：
CLL; NK; Anti-CD20 monoclonal antibodies; IL-8; ADCC; INCREASED SERUM-LEVELS; POOR-PROGNOSIS; GROWTH-FACTOR; NK CELLS; INTERLEUKIN-8; RITUXIMAB; ANTIBODY; CYTOTOXICITY; SURVIVAL; CLL;
D O I：
10.1016/j.leukres.2012.11.015
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Rituximab (RTX, anti-CD20 antibody) combined with chemotherapy is currently standard treatment for chronic lymphocytic leukemia (CLL). Serum level of IL-8 is a prognostic factor for CLL that correlates with disease stage. We investigated whether endogenous IL-8 affects RTX or Obinutuzumab (GA101) B-leukemic depletion mediated by natural killers (NK). Using whole peripheral blood lymphocytes from untreated CLL patients, RTX, but most significantly GA101, were effective in B-cell depletion and NK activation. IL-8 inhibition completely inhibited B-cell depletion by RTX and reduced GA101-induced B-cell depletion. Altogether results underline IL-8 as an endogenous NK co-activator and confirm GA101 therapeutic potential for CLL treatment. (c) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码：440 / 446
页数：7
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