DNA vaccines for the treatment of autoimmune disease

被引:35
作者
Ramshaw, IA
Fordham, SA
Bernard, CC
Maguire, D
Cowden, WB
Willenborg, DO
机构
[1] CANBERRA HOSP, NEUROSCI RES UNIT, CANBERRA, ACT, AUSTRALIA
[2] LA TROBE UNIV, FAC SCI & TECHNOL, NEUROIMMUNOL LAB, BUNDOORA, VIC 3083, AUSTRALIA
关键词
autoimmunity; DNA vaccines; experimental autoimmune encephalomyelitis;
D O I
10.1038/icb.1997.64
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
DNA vaccines represent one of the most significant developments in vaccine technology in recent years. Although, in general, studies have primarily focused on the induction of protective immune responses against infectious pathogens, the technology may prove useful for other immune-related diseases, including autoimmunity. Autoimmune disease results from a breakdown in tolerance to self antigens; however, the same fundamental immunological reactions that control immune responses to foreign antigens are also likely to operate during the course of autoimmune disease. These include the reciprocal regulation of Th cell subsets, Th1 cells appear to be involved in many organ-specific autoimmune diseases while suppression of disease is associated with cells of the Th2 phenotype. It has been possible, therefore, to suppress many of the pathological consequences of autoimmunity by manipulating the Th1/Th2 cell balance, The induction of Th2 responses by DNA immunization might therefore be expected to have a profound effect on the course of autoimmune disease. Indeed, we have demonstrated that DNA immunization can protect animals against the autoimmune central nervous system inflammatory disease, experimental autoimmune encephalomyelitis (EAE). As many other autoantigens have now been identified, the application of this technology to other autoimmune diseases warrants investigation.
引用
收藏
页码:409 / 413
页数:5
相关论文
共 44 条
[1]   ENCEPHALITOGENIC T-CELLS IN THE B10.PL MODEL OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS (EAE) ARE OF THE TH-1 LYMPHOKINE SUBTYPE [J].
ANDO, DG ;
CLAYTON, J ;
KONO, D ;
URBAN, JL ;
SERCARZ, EE .
CELLULAR IMMUNOLOGY, 1989, 124 (01) :132-143
[2]  
ATKINSON MA, 1994, NEW ENGL J MED, V331, P1428
[3]   ISLET-SPECIFIC T-CELL CLONES FROM THE NOD MOUSE RESPOND TO BETA-GRANULE ANTIGEN [J].
BERGMAN, B ;
HASKINS, K .
DIABETES, 1994, 43 (02) :197-203
[4]   DIRECT GENE-TRANSFER INTO SKELETAL-MUSCLE INVIVO - FACTORS AFFECTING EFFICIENCY OF TRANSFER AND STABILITY OF EXPRESSION [J].
DAVIS, HL ;
WHALEN, RG ;
DEMENEIX, BA .
HUMAN GENE THERAPY, 1993, 4 (02) :151-159
[5]  
DECARLI M, 1994, AUTOIMMUNITY, V18, P301
[6]   CYTOLYTIC T-CELLS WITH TH1-LIKE CYTOKINE PROFILE PREDOMINATE IN RETROORBITAL LYMPHOCYTIC INFILTRATES GRAVES OPHTHALMOPATHY [J].
DECARLI, M ;
DELIOS, MM ;
MARIOTTI, S ;
MARCOCCI, C ;
PINCHERA, A ;
RICCI, M ;
ROMAGNANI, S ;
DELPRETE, G .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1993, 77 (05) :1120-1124
[7]   EXAMINATION OF PARAMETERS AFFECTING THE ELICITATION OF HUMORAL IMMUNE-RESPONSES BY PARTICLE BOMBARDMENT-MEDIATED GENETIC IMMUNIZATION [J].
EISENBRAUN, MD ;
FULLER, DH ;
HAYNES, JR .
DNA AND CELL BIOLOGY, 1993, 12 (09) :791-797
[8]   INSULITIS IN TYPE-1 (INSULIN-DEPENDENT) DIABETES-MELLITUS IN MAN - MACROPHAGES, LYMPHOCYTES, AND INTERFERON-GAMMA CONTAINING CELLS [J].
FOULIS, AK ;
MCGILL, M ;
FARQUHARSON, MA .
JOURNAL OF PATHOLOGY, 1991, 165 (02) :97-103
[9]   EVIDENCE THAT THE T-CELL REPERTOIRE OF NORMAL RATS CONTAINS CELLS WITH THE POTENTIAL TO CAUSE DIABETES - CHARACTERIZATION OF THE CD4+ T-CELL SUBSET THAT INHIBITS THIS AUTOIMMUNE POTENTIAL [J].
FOWELL, D ;
MASON, D .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 177 (03) :627-636
[10]   A QUALITATIVE PROGRESSION IN HIV TYPE-1 GLYCOPROTEIN-120-SPECIFIC CYTOTOXIC CELLULAR AND HUMORAL IMMUNE-RESPONSES IN MICE RECEIVING A DNA-BASED GLYCOPROTEIN-120 VACCINE [J].
FULLER, DH ;
HAYNES, JR .
AIDS RESEARCH AND HUMAN RETROVIRUSES, 1994, 10 (11) :1433-1441