2004
DOI: 10.1097/01.tp.0000118410.61419.59
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Depleting Anti-Cd4 Monoclonal Antibody Cures New-Onset Diabetes, Prevents Recurrent Autoimmune Diabetes, and Delays Allograft Rejection in Nonobese Diabetic Mice1

Abstract: Our results provide the first evidence that newly established autoimmune islet destruction in NOD mice responds to a short course of anti-CD4 mAb. In contrast, costimulation blockade is ineffective in this clinically relevant model.

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Cited by 58 publications
(36 citation statements)
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“…While in most of these approaches mice were treated prior to or upon disease induction, only few were reported to be able to reverse established diabetes by acting on diabetogenic effector cells [31,32] or by harboring a dominant downregulatory mechanism [33]. In our studies, TAB4 functions through killing the disease-causing effector cells rather than through inducing a global immunosuppression.…”
Section: Discussionmentioning
confidence: 89%
“…While in most of these approaches mice were treated prior to or upon disease induction, only few were reported to be able to reverse established diabetes by acting on diabetogenic effector cells [31,32] or by harboring a dominant downregulatory mechanism [33]. In our studies, TAB4 functions through killing the disease-causing effector cells rather than through inducing a global immunosuppression.…”
Section: Discussionmentioning
confidence: 89%
“…Assuming that we can induce islet neogenesis in vivo, or efficiently expand b-cells in vitro, further advances in our understanding of the autoimmune process in type I diabetes [76][77][78][79] will help us to design strategies to prevent the autoimmune process from destroying the newly formed or transplanted islets or b-cells. Thus, secondary prevention as adjunctive therapy would be necessary for cell and gene therapy to succeed in reversing type I diabetes.…”
Section: Identification Of Islet Stem Cells and B-cell Progenitor Celmentioning
confidence: 99%
“…Second, the number of methods capable of stopping the progression of established disease is extremely limited, considerably less than those able to prevent disease onset. In fact, the ALS-, CD3-and CD4-specific antibodies are the only ones that have such a capacity [6,34,35]. This is a ma-jor fact since it relates to the clinical setting in which one would like to apply immunotherapy in T1D and, more importantly, recent data have proven that successful transfer to the clinic was obtained using one of these agents, i.e.…”
Section: Animal Models Of T1d May Be Predictive Of Human Applicationmentioning
confidence: 99%