Purpose of review

Grafted beta cells are lost because of recurrence of T1D and/or allograft rejection, two conditions diagnosed with pancreas graft biopsy, which is invasive and impossible in case of islet transplantation. This review synthetizes the current pathophysiological knowledge and discusses the interest of available immune biomarkers.

Recent findings

Despite the central role of auto-(recurrence of T1D) and allo-(T-cell mediated rejection) immune cellular responses, the latter are not directly monitored in routine. In striking contrast, there have been undisputable progresses in monitoring of auto and alloantibodies.

Summary

Except for pancreas recipients in whom anti-donor HLA antibodies can be directly responsible for antibody-mediated rejection, autoantibodies (and alloantibodies in islet recipients) have no direct pathogenic effect. However, their fluctuation offers a surrogate marker for the activation status of T cells (because antibody generation depends on T cells). This illustrates the necessity to understand the pathophysiology when interpreting a biomarker and selecting the appropriate treatment.

中文翻译：

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Beta细胞置换中的免疫学监测：朝着病理生理学指导的生物标志物的实现。

审查目的

由于T1D的复发和/或同种异体移植物的排斥，失去了已移植的β细胞，这是胰腺移植活检诊断出的两种情况，这是侵入性的，在胰岛移植的情况下是不可能的。这篇综述综合了当前的病理生理学知识，并讨论了可用免疫生物标志物的兴趣。

最近的发现

尽管自身（T1D复发）和同种（T细胞介导的排斥）免疫细胞反应起着核心作用，但常规情况下不能直接监测后者。与之形成鲜明对比的是，在监测自身抗体和同种抗体方面取得了无可争议的进展。

概括

除了抗胰岛HLA抗体可以直接导致抗体介导的排斥反应的胰腺受体外，自身抗体（和胰岛受体中的同种抗体）没有直接的致病作用。但是，它们的波动为T细胞的激活状态提供了替代标记（因为抗体的产生取决于T细胞）。这说明了在解释生物标志物并选择适当的治疗方法时必须了解病理生理学的必要性。