Preclinical evaluation of antigen-specific nanotherapy based on phosphatidylserine-liposomes for type 1 diabetes
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چکیده
منابع مشابه
Phosphatidylserine-Liposomes Promote Tolerogenic Features on Dendritic Cells in Human Type 1 Diabetes by Apoptotic Mimicry
Type 1 diabetes (T1D) is a metabolic disease caused by the autoimmune destruction of insulin-producing β-cells. With its incidence increasing worldwide, to find a safe approach to permanently cease autoimmunity and allow β-cell recovery has become vital. Relying on the inherent ability of apoptotic cells to induce immunological tolerance, we demonstrated that liposomes mimicking apoptotic β-cel...
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15 صفحه اولUse of Autoantigen-Loaded Phosphatidylserine-Liposomes to Arrest Autoimmunity in Type 1 Diabetes
INTRODUCTION The development of new therapies to induce self-tolerance has been an important medical health challenge in type 1 diabetes. An ideal immunotherapy should inhibit the autoimmune attack, avoid systemic side effects and allow β-cell regeneration. Based on the immunomodulatory effects of apoptosis, we hypothesized that apoptotic mimicry can help to restore tolerance lost in autoimmune...
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The identification and study of autoimmune diseases has taught us that recognition of selfantigens can have devastating consequences. Yet there is a paradox to autoreactivity: when correctly balanced, it is at the heart of robust self-tolerance. This concept gives rise to several questions. Can this balance be manipulated? And if so, by what means and through which mechanisms? What are the rule...
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A ntigen-based therapies (ABTs) seek to prevent or inhibit autoimmune diseases by inducing regulatory T-cell responses (active tolerance) or anergizing/deleting pathogenic T-cells (passive tolerance). The theoretical appeal of this therapeutic approach is that it may promote tolerance with little debilitation of the immune system. The clinical application of ABTs for autoimmune disease is still...
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ژورنال
عنوان ژورنال: Artificial Cells, Nanomedicine, and Biotechnology
سال: 2019
ISSN: 2169-1401,2169-141X
DOI: 10.1080/21691401.2019.1699812