Molecular mimicry between host and pathogen: examples from parasites and implication

被引:33
作者
Abu-Shakra, M
Buskila, D
Shoenfeld, Y [1 ]
机构
[1] Soroka Med Ctr, Rheumat Dis Unit, IL-84101 Beer Sheva, Israel
[2] Ben Gurion Univ Negev, IL-84105 Beer Sheva, Israel
[3] Chaim Sheba Med Ctr, Dept Med B, Autoimmune Dis Res Unit, IL-52621 Tel Hashomer, Israel
[4] Tel Aviv Univ, Sackler Fac Med, Tel Aviv, Israel
关键词
parasites; autoimmunity; molecular mimicry; autoantibodies;
D O I
10.1016/S0165-2478(99)00004-8
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 studies summarized in this paper suggest that parasites may trigger activation of autoimmune mechanisms. The association between parasites and autoimmunity could by manifested by the development of pathogenic anti-parasitic antibodies and cytotoxic T cells that attack and damage self tissues as a result of molecular mimicry between host and parasites. On the other hand, the homology between self and parasitic antigens may enable parasites to protect themselves from the immune system and to induce a state of immunosuppression. Although classic autoimmune diseases have not been shown to be more common amongst patients with chronic parasitic infections than in the general population, it is clear that autoimmune activity does occur in patients with chronic parasitic infections. It is possible that infection with parasites and other microbial agents may be followed by the activation of the immune system and, in genetically predisposed individuals, by loss of functional tolerance to self, activation of autoreactive cell that leads to progression to an overt autoimmune disease. (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:147 / 152
页数:6
相关论文
共 45 条
[1]  
Abu-Shakra M, 1991, Immunol Ser, V55, P285
[2]  
Abu-Shakra M, 1990, Hum Antibodies Hybridomas, V1, P10
[3]   PARASITIC INFECTION AND AUTOIMMUNITY [J].
ABUSHAKRA, M ;
SHOENFELD, Y .
AUTOIMMUNITY, 1991, 9 (04) :337-344
[4]  
ABUSHAKRA M, 1997, IDIOTYPES MED AUTOIM, P53
[5]   THE SUSCEPTIBILITY SEQUENCE TO RHEUMATOID-ARTHRITIS IS A CROSS-REACTIVE B-CELL EPITOPE SHARED BY THE ESCHERICHIA-COLI HEAT-SHOCK PROTEIN DNAJ AND THE HISTOCOMPATIBILITY LEUKOCYTE ANTIGEN DRB10401 MOLECULE [J].
ALBANI, S ;
TUCKWELL, JE ;
ESPARZA, L ;
CARSON, DA ;
ROUDIER, J .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 89 (01) :327-331
[6]  
ARGOV S, 1989, CLIN EXP IMMUNOL, V76, P190
[7]  
Avila Jose Luis, 1992, Acta Cientifica Venezolana, V43, P330
[8]   Molecular mimicry and T cell-mediated autoimmune disease [J].
Barnaba, V ;
Sinigaglia, F .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 185 (09) :1529-1531
[9]   PARASITE EXPOSURE ELICITS A PREFERENTIAL T-CELL RESPONSE INVOLVED IN PROTECTIVE IMMUNITY AGAINST EIMERIA SPECIES IN CHICKENS PRIMED BY AN INTERNAL-IMAGE ANTI-IDIOTYPIC ANTIBODY [J].
BHOGAL, BS ;
JACOBSON, EB ;
TSE, HY ;
SCHMATZ, DM ;
RAVINO, OJ .
INFECTION AND IMMUNITY, 1989, 57 (09) :2804-2810
[10]   MOLECULAR MIMICRY IN THE PATHOGENESIS OF AIDS - THE HIV MHC MYCOPLASMA TRIANGLE [J].
BISSET, LR .
MEDICAL HYPOTHESES, 1994, 43 (06) :388-396