Resolution of chronic inflammation by therapeutic induction of apoptosis

被引:44
作者
Anderson, GP [1 ]
机构
[1] CIBA GEIGY AG,ASTHMA & ALLERGY RES,CH-4002 BASEL,SWITZERLAND
关键词
D O I
10.1016/S0165-6147(96)01004-8
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
[No abstract available]
引用
收藏
页码:438 / 442
页数:5
相关论文
共 27 条
[1]   FAS TRANSDUCES ACTIVATION SIGNALS IN NORMAL HUMAN T-LYMPHOCYTES [J].
ALDERSON, MR ;
ARMITAGE, RJ ;
MARASKOVSKY, E ;
TOUGH, TW ;
ROUX, E ;
SCHOOLEY, K ;
RAMSDELL, F ;
LYNCH, DH .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 178 (06) :2231-2235
[2]   T-CELL RECEPTOR-INDUCED FAS LIGAND EXPRESSION IN CYTOTOXIC T-LYMPHOCYTE CLONES IS BLOCKED BY PROTEIN-TYROSINE KINASE INHIBITORS AND CYCLOSPORINE-A [J].
ANEL, A ;
BUFERNE, M ;
BOYER, C ;
SCHMITTVERHULST, AM ;
GOLSTEIN, P .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1994, 24 (10) :2469-2476
[3]   ON THE CELLULAR BASIS OF IMMUNOLOGICAL T-CELL MEMORY [J].
BRUNO, L ;
KIRBERG, J ;
VONBOEHMER, H .
IMMUNITY, 1995, 2 (01) :37-43
[4]   FADD, A NOVEL DEATH DOMAIN-CONTAINING PROTEIN, INTERACTS WITH THE DEATH DOMAIN OF FAS AND INITIATES APOPTOSIS [J].
CHINNAIYAN, AM ;
OROURKE, K ;
TEWARI, M ;
DIXIT, VM .
CELL, 1995, 81 (04) :505-512
[5]   A FAS-ASSOCIATED PROTEIN FACTOR, FAF1, POTENTIATES FAS-MEDIATED APOPTOSIS [J].
CHU, KT ;
NIU, XH ;
WILLIAMS, LT .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (25) :11894-11898
[6]  
EISCHEN CM, 1994, J IMMUNOL, V153, P1947
[7]   FAS-INDUCED APOPTOSIS IS MEDIATED VIA A CERAMIDE-INITIATED RAS SIGNALING PATHWAY [J].
GULBINS, E ;
BISSONNETTE, R ;
MAHBOUBI, A ;
MARTIN, S ;
NISHIOKA, W ;
BRUNNER, T ;
BAIER, G ;
BAIERBITTERLICH, G ;
BYRD, C ;
LANG, F ;
KOLESNICK, R ;
ALTMAN, A ;
GREEN, D .
IMMUNITY, 1995, 2 (04) :341-351
[8]   EOSINOPHIL HEMATOPOIETINS ANTAGONIZE THE PROGRAMMED CELL-DEATH OF EOSINOPHILS - CYTOKINE AND GLUCOCORTICOID EFFECTS ON EOSINOPHILS MAINTAINED BY ENDOTHELIAL-CELL CONDITIONED MEDIUM [J].
HER, E ;
FRAZER, J ;
AUSTEN, KF ;
OWEN, WF .
JOURNAL OF CLINICAL INVESTIGATION, 1991, 88 (06) :1982-1987
[9]   BCL-2 IS AN INNER MITOCHONDRIAL-MEMBRANE PROTEIN THAT BLOCKS PROGRAMMED CELL-DEATH [J].
HOCKENBERY, D ;
NUNEZ, G ;
MILLIMAN, C ;
SCHREIBER, RD ;
KORSMEYER, SJ .
NATURE, 1990, 348 (6299) :334-336
[10]  
ITOH N, 1993, J IMMUNOL, V151, P621