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1
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0028037782
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Regulatory T cell clones induced by oral tolerance: suppression of autoimmune encephalomyelitis
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of outstanding interest, Shows that following induction of oral tolerance to MBP, clones can be isolated that produce Th2-type cytokines. These clones are able to protect from induction of EAE by immunization with MBP, and can also downregulate ongoing EAE. The relative contribution of IL-4, IL-10 or transforming growth factor-β to the ability of the clones to regulate disease remains unclear.
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(1994)
Science
, vol.265
, pp. 1237-1240
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Chen1
Kuchroo2
Inobe3
Hafler4
Weiner5
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6
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0028966091
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Prevention of experimental autoimmune encephalomyelitis by antibodies against interleukin 12
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of special interest, In contrast to the administration of IL-12, which exacerbated the EAE induced by transfer of PLP clones, the administration of anti-IL-12 antibody inhibited the development of EAE. This shows that the dependence on IL-12 in the development of EAE may continue after initial stages.
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(1995)
J Exp Med
, vol.181
, pp. 381-386
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Leonard1
Waldburger2
Goldman3
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11
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0028926524
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Interleukin 12 administration induces T helper type 1 cells and accelerates autoimmune diabetes in NOD mice
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+ 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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(1995)
J Exp Med
, vol.181
, pp. 817-821
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Trembleau1
Penna2
Bosi3
Mortara4
Gately5
Adorini6
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12
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0029030964
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T helper cell subsets in insulin-dependent diabetes
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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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(1995)
Science
, vol.268
, pp. 1185-1188
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Katz1
Benoist2
Mathis3
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13
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0028914351
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Epitope specificity, cytokine production profile and diabetogenic activity of insulin-specific T cell clones isolated from NOD mice
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(1995)
Eur J Immunol
, vol.25
, pp. 1056-1062
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Daniel1
Gill2
Schloot3
Wegmann4
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21
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0027971672
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IL-12 stimulates the development of acute graft-versus-host disease in mice that normally would develop chronic, autoimmune graft-versus-host disease
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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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(1994)
J Immunol
, vol.153
, pp. 4040-4047
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Via1
Rus2
Gately3
Finkelman4
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28
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0028306935
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Epitope and functional specificity of peripheral tolerance induction in experimental autoimmune encephalomyelitis in adult Lewis rats
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(1994)
J Immunol
, vol.153
, pp. 841-851
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Malotky1
Pope2
Miller3
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30
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0028146261
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Antigen-driven tissue-specific suppression following oral tolerance: orally administered myelin basic protein suppresses proteolipid protein-induced experimental autoimmune encephalomyelitis in the SJL mouse
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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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(1994)
Eur J Immunol
, vol.24
, pp. 2104-2109
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Al-Sabbagh1
Miller2
Santos3
Weiner4
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32
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0028949152
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2 developmental pathways: application to autoimmune disease therapy
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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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(1995)
Cell
, vol.80
, pp. 707-718
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Kuchroo1
Das2
Brown3
Ranger4
Zamvil5
Sobel6
Weiner7
Nabavi8
Glimcher9
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33
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0028900297
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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
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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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(1995)
J Exp Med
, vol.181
, pp. 1145-1155
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Lenschow1
Ho2
Sattar3
Rhee4
Gray5
Nabavi6
Herold7
Bluestone8
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36
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0028346888
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Production of interleukin 10 by islet cells accelerates immune-mediated destruction of beta cells in nonobese diabetic mice
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(1994)
J Exp Med
, vol.179
, pp. 1379-1384
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Wogensen1
Lee2
Sarvetnick3
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39
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0028409436
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A role for non-MHC genetic polymorphism in susceptibility to spontaneous autoimmunity
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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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(1994)
Immunity
, vol.1
, pp. 73-83
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Scott1
Liblau2
Degermann3
Marconi4
Ogata5
Caton6
McDevitt7
Lo8
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41
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0028344855
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Acetylcholine receptor-reactive T cells in myasthenia gravis: evidence for the involvement of different subpopulations of T helper cells
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(1994)
J Neuroimmunol
, vol.50
, pp. 177-186
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Yi1
Ahlberg2
Pirskanen3
Lefvert4
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49
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0028105040
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*0602 does not prevent them
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*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.
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(1994)
J Autoimmun
, vol.7
, pp. 889-897
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Huang1
She2
Muir3
Laskowska4
Zorovich5
Schatz6
Maclaren7
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50
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0028035382
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Quantitation of glutamic acid decarboxylase autoantibody levels in prospectively evaluated relatives of patients with type I diabetes
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(1994)
Diabetes
, vol.43
, pp. 1229-1233
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Yu1
Gianani2
Eisenbarth3
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