MURINE B7-2, AN ALTERNATIVE CTLA4 COUNTER-RECEPTOR THAT COSTIMULATES T-CELL PROLIFERATION AND INTERLEUKIN-2 PRODUCTION

被引:368
作者
FREEMAN, GJ
BORRIELLO, F
HODES, RJ
REISER, H
GRIBBEN, JG
NG, JW
KIM, J
GOLDBERG, JM
HATHCOCK, K
LASZLO, G
LOMBARD, LA
WANG, S
GRAY, GS
NADLER, LM
SHARPE, AH
机构
[1] HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115
[2] REPLIGEN CORP,CAMBRIDGE,MA 02139
[3] BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV IMMUNOL RES,BOSTON,MA 02115
[4] HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115
[5] NIA,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892
[6] NCI,BETHESDA,MD 20892
关键词
D O I
10.1084/jem.178.6.2185
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The B7-1 molecule, expressed on antigen presenting cells (APC), provides a crucial costimulatory signal for T cell activation. Recent studies demonstrate the existence of alternative, non-B7-1 CTLA4 counter-receptors in mice and humans. Here, we describe the molecular cloning and demonstrate costimulatory function of the murine B7-2 (mB7-2) gene. Murine B7-2 cDNA encodes a member of the Ig supergene family that binds CTLA4-Ig and stains with the GL1 but not anti-mB7-1 mAb. Murine B7-2 costimulates the proliferation and interleukin 2 production of CD4+ T cells and this costimulation can be inhibited by either CTLA4-Ig or GL1 mAb. Identification of the B7-2 molecule will permit further manipulation of the B7:CD28/CTLA4 costimulatory pathway which has been shown to be involved in the prevention of tolerance, induction of tumor immunity, and most recently, in the pathogenesis of autoimmunity.
引用
收藏
页码:2185 / 2192
页数:8
相关论文
共 32 条
[1]   MOLECULAR-CLONING OF A CD28 CDNA BY A HIGH-EFFICIENCY COS CELL EXPRESSION SYSTEM [J].
ARUFFO, A ;
SEED, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (23) :8573-8577
[2]   CONSTITUTIVE EXPRESSION OF B7 RESTORES IMMUNOGENICITY OF TUMOR-CELLS EXPRESSING TRUNCATED MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II MOLECULES [J].
BASKAR, S ;
OSTRANDROSENBERG, S ;
NABAVI, N ;
NADLER, LM ;
FREEMAN, GJ ;
GLIMCHER, LH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (12) :5687-5690
[3]   REVERSAL OF INVITRO T-CELL CLONAL ANERGY BY IL-2 STIMULATION [J].
BEVERLY, B ;
KANG, SM ;
LENARDO, MJ ;
SCHWARTZ, RH .
INTERNATIONAL IMMUNOLOGY, 1992, 4 (06) :661-671
[4]   B7 BUT NOT INTERCELLULAR-ADHESION MOLECULE-1 COSTIMULATION PREVENTS THE INDUCTION OF HUMAN ALLOANTIGEN-SPECIFIC TOLERANCE [J].
BOUSSIOTIS, VA ;
FREEMAN, GJ ;
GRAY, G ;
GRIBBEN, J ;
NADLER, LM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 178 (05) :1753-1763
[5]  
BOUSSIOTIS VA, 1993, IN PRESS P NATL ACAD
[6]   COSTIMULATION OF ANTITUMOR IMMUNITY BY THE B7 COUNTERRECEPTOR FOR THE LYMPHOCYTE-T MOLECULES CD28 AND CTLA-4 [J].
CHEN, LP ;
ASHE, S ;
BRADY, WA ;
HELLSTROM, I ;
HELLSTROM, KE ;
LEDBETTER, JA ;
MCGOWAN, P ;
LINSLEY, PS .
CELL, 1992, 71 (07) :1093-1102
[7]  
FREEMAN GJ, 1989, J IMMUNOL, V143, P2714
[8]  
FREEMAN GJ, 1992, J IMMUNOL, V149, P3795
[9]   STRUCTURE, EXPRESSION, AND T-CELL COSTIMULATORY ACTIVITY OF THE MURINE HOMOLOG OF THE HUMAN LYMPHOCYTE-B ACTIVATION ANTIGEN-B7 [J].
FREEMAN, GJ ;
GRAY, GS ;
GIMMI, CD ;
LOMBARD, DB ;
ZHOU, LJ ;
WHITE, M ;
FINGEROTH, JD ;
GRIBBEN, JG ;
NADLER, LM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 174 (03) :625-631
[10]  
FREEMAN GJ, 1993, IN PRESS SCIENCE WAS