Survival signals in leukemic large granular lymphocytes

被引:38
作者
Epling-Burnette, PK
Loughran, TP
机构
[1] Univ S Florida, H Lee Moffit Canc Ctr & Res Inst, Hematol Malignancy Program, Tampa, FL 33612 USA
[2] James A Haley Vet Adm Med Ctr, Tampa, FL 33612 USA
关键词
D O I
10.1016/S0037-1963(03)00135-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The central hypothesis of our laboratory research program in large granular lymphocyte (LGL) leukemia is that leukemic LGL represent antigen-driven cytotoxic T lymphocytes (CTL) with characteristics of dysregulated apoptosis. The clinical features of LGL leukemia highlight the association of autoimmune diseases such as rheumatoid arthritis with the T-cell form of LGL leukemia. We therefore used LGL leukemia as a model disease of dysregulated apoptosis leading to both malignant and autoimmune diseases. Here, we review our understanding of survival signals activated in leukemic LGL in the context of knowledge concerning apoptotic pathways in activated normal lymphocytes. © 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:213 / 220
页数:8
相关论文
共 108 条
[31]  
Holmström TH, 1999, MOL CELL BIOL, V19, P5991
[32]   MAPK/ERK signaling in activated T cells inhibits CD95/Fas-mediated apoptosis downstream of DISC assembly [J].
Holmström, TH ;
Schmitz, I ;
Söderström, TS ;
Poukkula, M ;
Johnson, VL ;
Chow, SC ;
Krammer, PH ;
Eriksson, JE .
EMBO JOURNAL, 2000, 19 (20) :5418-5428
[33]  
Hu SM, 1997, J BIOL CHEM, V272, P9621
[34]   I-FLICE, a novel inhibitor of tumor necrosis factor receptor-1- and CD-95-induced apoptosis [J].
Hu, SM ;
Vincenz, C ;
Ni, J ;
Gentz, R ;
Dixit, VM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (28) :17255-17257
[35]   Inhibition of death receptor signals by cellular FLIP [J].
Irmler, M ;
Thome, M ;
Hahne, M ;
Schneider, P ;
Hofmann, B ;
Steiner, V ;
Bodmer, JL ;
Schroter, M ;
Burns, K ;
Mattmann, C ;
Rimoldi, D ;
French, LE ;
Tschopp, J .
NATURE, 1997, 388 (6638) :190-195
[36]   THE POLYPEPTIDE ENCODED BY THE CDNA FOR HUMAN CELL-SURFACE ANTIGEN FAS CAN MEDIATE APOPTOSIS [J].
ITOH, N ;
YONEHARA, S ;
ISHII, A ;
YONEHARA, M ;
MIZUSHIMA, S ;
SAMESHIMA, M ;
HASE, A ;
SETO, Y ;
NAGATA, S .
CELL, 1991, 66 (02) :233-243
[37]   FAS(CD95) FASL INTERACTIONS REQUIRED FOR PROGRAMMED CELL-DEATH AFTER T-CELL ACTIVATION [J].
JU, ST ;
PANKA, DJ ;
CUI, HL ;
ETTINGER, R ;
ELKHATIB, M ;
SHERR, DH ;
STANGER, BZ ;
MARSHAKROTHSTEIN, A .
NATURE, 1995, 373 (6513) :444-448
[38]  
KASTENSPORTES C, 1994, BLOOD, V83, P767
[39]   CYTOTOXICITY-DEPENDENT APO-1 (FAS/CD95)-ASSOCIATED PROTEINS FORM A DEATH-INDUCING SIGNALING COMPLEX (DISC) WITH THE RECEPTOR [J].
KISCHKEL, FC ;
HELLBARDT, S ;
BEHRMANN, I ;
GERMER, M ;
PAWLITA, M ;
KRAMMER, PH ;
PETER, ME .
EMBO JOURNAL, 1995, 14 (22) :5579-5588
[40]   Levels of soluble Fas/APO-1/CD95 in systemic lupus erythematosus and juvenile rheumatoid arthritis [J].
Knipping, E ;
Krammer, PH ;
Onel, KB ;
Lehman, TJA ;
Mysler, E ;
Elkon, KB .
ARTHRITIS AND RHEUMATISM, 1995, 38 (12) :1735-1737