Genetic basis of murine lupus

被引:78
作者
Santiago-Raber, ML
Laporte, C
Reininger, L
Izui, S [1 ]
机构
[1] Ctr Med Univ Geneva, Dept Pathol, CH-1211 Geneva 4, Switzerland
[2] Fac Med Marseille, INSERM, U399, F-13385 Marseille 05, France
关键词
systemic lupus erythematosus; genetic linkage analysis; murine models; genes of autoimmunity;
D O I
10.1016/S1568-9972(03)00062-4
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by the formation of a variety of autoantibodies and subsequent development of severe glomerulonephritis. Etiology of SLE remains unknown even if it is now well established that SLE is under polygenic control as well as the contribution of hormonal and environmental factors. The availability of several murine strains that spontaneously develop an autoimmune syndrome resembling human SLE, such as New Zealand, MRL and BXSB mice has provided useful tools for the genetic dissection of susceptibility to SLE. Moreover, development of various transgenic and mutant mice has made it possible to identify a number of susceptibility genes such as those involved in the regulation of apoptosis or B cell receptor signaling that can trigger lupus-like phenotypes. Obviously, further identification of the genetic defects present in lupus-prone mice is of paramount importance for understanding the immunopathogenesis of SLE. (C) 2003 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:33 / 39
页数:7
相关论文
共 44 条
  • [1] Serum amyloid P component controls chromatin degradation and prevents antinuclear autoimmunity
    Bickerstaff, MCM
    Botto, M
    Hutchinson, WL
    Herbert, J
    Tennent, GA
    Bybee, A
    Mitchell, DA
    Cook, HT
    Butler, PJG
    Walport, MJ
    Pepys, MB
    [J]. NATURE MEDICINE, 1999, 5 (06) : 694 - 697
  • [2] IDENTIFICATION OF PTP1C MUTATION AS THE GENETIC-DEFECT IN MOTH-EATEN AND VIABLE MOTH-EATEN MICE - A STEP TOWARD DEFINING THE ROLES OF PROTEIN-TYROSINE PHOSPHATASES IN THE REGULATION OF HEMATOPOIETIC-CELL DIFFERENTIATION AND FUNCTION
    BIGNON, JS
    SIMINOVITCH, KA
    [J]. CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1994, 73 (02): : 168 - 179
  • [3] Spontaneous autoimmune disease in FcγRIIB-deficient mice results from strain-specific epistasis
    Bolland, S
    Ravetch, JV
    [J]. IMMUNITY, 2000, 13 (02) : 277 - 285
  • [4] Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies
    Botto, M
    Dell'Agnola, C
    Bygrave, AE
    Thompson, EM
    Cook, HT
    Petry, F
    Loos, M
    Pandolfi, PP
    Walport, MJ
    [J]. NATURE GENETICS, 1998, 19 (01) : 56 - 59
  • [5] LPR AND GLD - SINGLE GENE MODELS OF SYSTEMIC AUTOIMMUNITY AND LYMPHOPROLIFERATIVE DISEASE
    COHEN, PL
    EISENBERG, RA
    [J]. ANNUAL REVIEW OF IMMUNOLOGY, 1991, 9 : 243 - 269
  • [6] Impaired Fas response and autoimmunity in Pten+/- mice
    Di Cristofano, A
    Kotsi, P
    Peng, YF
    Cordon-Cardo, C
    Elkon, KB
    Pandolfi, PP
    [J]. SCIENCE, 1999, 285 (5436) : 2122 - 2125
  • [7] GENETIC-ANALYSIS OF THE NZB CONTRIBUTION TO LUPUS-LIKE AUTOIMMUNE-DISEASE IN (NZB X NZW)F-1 MICE
    DRAKE, CG
    BABCOCK, SK
    PALMER, E
    KOTZIN, BL
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (09) : 4062 - 4066
  • [8] DRAKE CG, 1995, J IMMUNOL, V154, P2441
  • [9] Gu LJ, 1998, J IMMUNOL, V161, P6999
  • [10] Haywood MEK, 2000, ARTHRITIS RHEUM, V43, P349, DOI 10.1002/1529-0131(200002)43:2<349::AID-ANR14>3.0.CO