Immunodeficiencies caused by genetic defects in protein kinases

被引:15
作者
Notarangelo, LD
机构
[1] Department of Pediatrics, University of Brescia, Brescia
关键词
D O I
10.1016/S0952-7915(96)80028-8
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 recognition that defects of ZAP-70 and, more recently, of JAK3 kinase in humans result in severe combined immunodeficiency, and the demonstration that targeting of these and other protein-kinase genes in mice also leads to immunodeficiency, have highlighted the crucial role that these proteins play in T-cell differentiation and activation.
引用
收藏
页码:448 / 453
页数:6
相关论文
共 56 条
[1]   DEFECTIVE T-CELL RECEPTOR SIGNALING IN MICE LACKING THE THYMIC ISOFORM OF P59(FYN) [J].
APPLEBY, MW ;
GROSS, JA ;
COOKE, MP ;
LEVIN, SD ;
QIAN, X ;
PERLMUTTER, RM .
CELL, 1992, 70 (05) :751-763
[2]   DEFECTIVE T-CELL RECEPTOR SIGNALING AND CD8(+) THYMIC SELECTION IN HUMANS LACKING ZAP-70 KINASE [J].
ARPAIA, E ;
SHAHAR, M ;
DADI, H ;
COHEN, A ;
ROIFMAN, CM .
CELL, 1994, 76 (05) :947-958
[3]   CD28 IS ASSOCIATED WITH AND INDUCES THE IMMEDIATE TYROSINE PHOSPHORYLATION AND ACTIVATION OF THE TEC FAMILY KINASE ITK/EMT IN THE HUMAN JURKAT LEUKEMIC T-CELL LINE [J].
AUGUST, A ;
GIBSON, S ;
KAWAKAMI, Y ;
KAWAKAMI, T ;
MILLS, GB ;
DUPONT, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (20) :9347-9351
[4]   DEFECTIVE DNA-DEPENDENT PROTEIN-KINASE ACTIVITY IS LINKED TO V(D)J RECOMBINATION AND DNA-REPAIR DEFECTS ASSOCIATED WITH THE MURINE SCID MUTATION [J].
BLUNT, T ;
FINNIE, NJ ;
TACCIOLI, GE ;
SMITH, GCM ;
DEMENGEOT, J ;
GOTTLIEB, TM ;
MIZUTA, R ;
VARGHESE, AJ ;
ALT, FW ;
JEGGO, PA ;
JACKSON, SP .
CELL, 1995, 80 (05) :813-823
[5]   PROTEIN-TYROSINE KINASES IN THE INITIATION OF ANTIGEN RECEPTOR SIGNALING [J].
BOLEN, JB .
CURRENT OPINION IN IMMUNOLOGY, 1995, 7 (03) :306-311
[6]   THE SCID MOUSE MUTANT - DEFINITION, CHARACTERIZATION, AND POTENTIAL USES [J].
BOSMA, MJ ;
CARROLL, AM .
ANNUAL REVIEW OF IMMUNOLOGY, 1991, 9 :323-350
[7]   COMPLEMENTATION OF THE IONIZING-RADIATION SENSITIVITY, DNA END BINDING, AND V(D)J RECOMBINATION DEFECTS OF DOUBLE-STRAND BREAK REPAIR MUTANTS BY THE P86 KU AUTOANTIGEN [J].
BOUBNOV, NV ;
HALL, KT ;
WILLS, Z ;
LEE, SE ;
HE, DM ;
BENJAMIN, DM ;
PULASKI, CR ;
BAND, H ;
REEVES, W ;
HENDRICKSON, EA ;
WEAVER, DT .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (03) :890-894
[8]  
BOUBNOV NV, 1995, MOL CELL BIOL, V15, P5700
[9]   PREVENTION OF T-CELL ANERGY BY SIGNALING THROUGH THE GAMMA(C) CHAIN OF THE IL-2 RECEPTOR [J].
BOUSSIOTIS, VA ;
BARBER, DL ;
NAKARAI, T ;
FREEMAN, GJ ;
GRIBBEN, JG ;
BERNSTEIN, GM ;
DANDREA, AD ;
RITZ, J ;
NADLER, LM .
SCIENCE, 1994, 266 (5187) :1039-1042
[10]   DEFECTIVE LYMPHOID DEVELOPMENT IN MICE LACKING EXPRESSION OF THE COMMON CYTOKINE RECEPTOR-GAMMA CHAIN [J].
CAO, XQ ;
SHORES, EW ;
HULI, J ;
ANVER, MR ;
KELSALL, BL ;
RUSSELL, SM ;
DRAGO, J ;
NOGUCHI, M ;
GRINBERG, A ;
BLOOM, ET ;
PAUL, WE ;
KATZ, SI ;
LOVE, PE ;
LEONARD, WJ .
IMMUNITY, 1995, 2 (03) :223-238