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Volumn 7, Issue 6, 1995, Pages 793-798

The Th1/Th2 balance in autoimmunity

Author keywords

[No Author keywords available]

Indexed keywords

CD4 ANTIGEN;

EID: 0029619257     PISSN: 09527915     EISSN: None     Source Type: Journal    
DOI: 10.1016/0952-7915(95)80050-6     Document Type: Article
Times cited : (191)

References (51)
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    • Interleukin 12 administration induces T helper type 1 cells and accelerates autoimmune diabetes in NOD mice
    • + T cells. This is strong evidence that the destructive autoimmune response in NOD mice is Th1 mediated and, furthermore, in male NOD mice that do not normally develop diabetes, disease was induced by administration of IL-12. This suggests that the non-destructive autoimmunity in these mice is mediated by a Th2-like response that controls the potentially damaging Th1 cells.
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    • T helper cell subsets in insulin-dependent diabetes
    • of outstanding interest, Transfer of diabetes by a Th1 clone specific for an unidentified β-cell antigen. As in EAE, a Th2 clone specific for the same antigen was unable to transfer diabetes; unlike the finding for EAE, the Th2 clone did not protect from disease transfer by the Th1 clone.
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    • of special interest, Transfer of parental splenocytes to F1 neonates causes chronic autoimmune disease as a result of graft-versus-host disease. Administration of IL-12 within seven days, but not later, prevents this and instead induces an anti-host cytotoxic T lymphocyte response. Thus, a Th2-mediated autoimmune disease is prevented by generating a Th1 response instead.
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    • Self-reactive anti-class II T helper type 2 cell lines derived from gold salt-injected rats trigger B cell polyclonal activation and transfer autoimmunity in CD8-depleted normal syngeneic recipients
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    • of special interest, Demonstration that oral tolerance, which appears to induce Th2 regulatory cells, does not have to utilize the immunizing antigen. Oral antigen administration can influence the response to anatomically adjacent antigens, in this case PLP and MBP. This is a potentially important observation for future therapeutic approaches.
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    • of outstanding interest, Demonstration that it might be possible to influence the Th1/Th2 bias by administration of antigen plus anti-B7-1 or B7-2 antibodies. In a model of EAE, anti-B7-1 induced a disease-preventing Th2 response, whereas anti-B7-2 exacerbated the disease by producing a Th1 response. Also, further demonstrates that Th2 clones can downregulate an ongoing Th1 response.
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    • Differential effects of anti-B7-1 and anti-B7-2 monoclonal antibody treatment on the development of diabetes in the nonobese diabetic mouse
    • of outstanding interest, of special interest, Shows that in a spontaneous model of IDDM (the NOD mouse) antibodies to B7-1 and B7-2 have different effects on development of disease. Anti-B7-1 accelerated disease progression and induced disease in resistant male mice. In contrast, anti-B7-2 prevented disease development. This appears to be at odds with the findings of Kuchroo et al. [32] who studied the EAE model, and suggests that further work on the antibodies mechanism of action is necessary.
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  • 39
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    • A role for non-MHC genetic polymorphism in susceptibility to spontaneous autoimmunity
    • of special interest, Diabetes induced by crossing transgenic β cell HA mice with HA-specific TCR transgenic mice was studied on different non-MHC backgrounds. The non-MHC background determined whether autoimmunity or autoimmune disease (diabetes) developed. Indirect evidence suggests that the destructive response is Th1 dependent and that non MHC genes influence the Th1/Th2 bias of an autoimmune response.
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    • *0602 does not prevent them
    • *0602 protects otherwise genetically at risk individuals from IDDM, it has no effect on the production of β-cell specific autoantibodies. This is substantial evidence that an ongoing balance of Th1/Th2 responses occurs in β cell autoimmune responses.
    • (1994) J Autoimmun , vol.7 , pp. 889-897
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* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.