Endogenous retroviral sequences in the pathogenesis of systemic autoimmune disease

被引:6
作者
Walchner, M
LeibMosch, C
Messer, G
Germaier, H
Plewig, G
Kind, P
机构
[1] UNIV HEIDELBERG, KLINIKUM MANNHEIM, MED CLIN 3, HEIDELBERG, GERMANY
[2] GSF MUNICH, NATL RES CTR ENVIRONM & HLTH, INST MOL VIROL, NEUHERBERG, GERMANY
关键词
D O I
10.1001/archderm.133.6.767
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Objectives: To update information on endogenous retroviral, sequences and discuss their role in systemic autoimmune disease. Data Sources: Articles retrieved after MEDLINE search and personal communications and cooperation with the Institute of Virology. Data Synthesis: There are 2 modes of pathogenetic mechanisms through which endogenous retroviral sequences could cause systemic autoimmune disease: expression of endogenous retroviral gene products sharing antigenic determinants with cellular proteins; and activation or destruction of cellular genes as a consequence of insertional mutagenesis. Both mechanisms have been demonstrated in vitro and in vivo in animal models. Conclusion: Investigations on endogenous retroviral sequences in humans may offer new insights into the pathogenesis of autoimmune disease.
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收藏
页码:767 / 771
页数:5
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共 69 条
[1]  
AHMED SA, 1985, AM J PATHOL, V121, P531
[2]   HUMAN T-CELL LYMPHOTROPIC VIRUS (HTLV)-RELATED ENDOGENOUS SEQUENCE, HRES-1, ENCODES A 28-KDA PROTEIN - A POSSIBLE AUTOANTIGEN FOR HTLV-I GAG-REACTIVE AUTOANTIBODIES [J].
BANKI, K ;
MACEDA, J ;
HURLEY, E ;
ABLONCZY, E ;
MATTSON, DH ;
SZEGEDY, L ;
HUNG, C ;
PERL, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (05) :1939-1943
[3]   MECHANISMS OF AUTOIMMUNE-DISEASE INDUCTION - THE ROLE OF THE IMMUNE-RESPONSE TO MICROBIAL PATHOGENS [J].
BEHAR, SM ;
PORCELLI, SA .
ARTHRITIS AND RHEUMATISM, 1995, 38 (04) :458-476
[4]   HIV ENV GLYCOPROTEIN SHARES A CROSS-REACTING EPITOPE WITH A SURFACE PROTEIN PRESENT ON ACTIVATED HUMAN-MONOCYTES AND INVOLVED IN ANTIGEN PRESENTATION [J].
BERETTA, A ;
GRASSI, F ;
PELAGI, M ;
CLIVIO, A ;
PARRAVICINI, C ;
GIOVINAZZO, G ;
ANDRONICO, F ;
LOPALCO, L ;
VERANI, P ;
BUTTO, S ;
TITTI, F ;
ROSSI, GB ;
VIALE, G ;
GINELLI, E ;
SICCARDI, AG .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1987, 17 (12) :1793-1798
[5]   INCREASED ANTIRETROVIRAL ANTIBODY REACTIVITY IN SERA FROM A DEFINED POPULATION OF PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS - CORRELATION WITH AUTOANTIBODIES AND CLINICAL MANIFESTATIONS [J].
BLOMBERG, J ;
NIVED, O ;
PIPKORN, R ;
BENGTSSON, A ;
ERLINGE, D ;
STURFELT, G .
ARTHRITIS AND RHEUMATISM, 1994, 37 (01) :57-66
[6]   NUCLEOTIDE AND AMINO-ACID HOMOLOGY BETWEEN THE HUMAN THYROTROPIN RECEPTOR AND THE HIV-1 NEF PROTEIN - IDENTIFICATION AND FUNCTIONAL-ANALYSIS [J].
BURCH, HB ;
NAGY, EV ;
LUKES, YG ;
CAI, WY ;
WARTOFSKY, L ;
BURMAN, KD .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1991, 181 (01) :498-505
[7]  
CALLAHAN R, 1988, BANBURY REPORT, V30, P91
[8]  
Cheevers W P, 1988, Adv Virus Res, V34, P189, DOI 10.1016/S0065-3527(08)60518-7
[9]   LOCALIZATION OF B-CELL STIMULATORY ACTIVITY OF HIV-1 TO THE CARBOXYL TERMINUS OF GP41 [J].
CHIRMULE, N ;
KALYANARAMAN, VS ;
SAXINGER, C ;
WONGSTAAL, F ;
GHRAYEB, J ;
PAHWA, S .
AIDS RESEARCH AND HUMAN RETROVIRUSES, 1990, 6 (03) :299-305
[10]   A T(H)1-]T(H)2 SWITCH IS A CRITICAL STEP IN THE ETIOLOGY OF HIV-INFECTION [J].
CLERICI, M ;
SHEARER, GM .
IMMUNOLOGY TODAY, 1993, 14 (03) :107-110