High titers of pathogenic autoantibodies are a hallmark of many autoimmune diseases. However, much remains unknown about the self-reactive plasma cells that are key mediators of disease. We propose a model in which the varying efficacy of precursor B cell depletion for the treatment of humoral autoimmunity can be explained by differences in the relative contributions of pathogenic antibodies by short-lived versus long-lived plasma cells. Beyond therapeutic considerations, this model suggests that we can infer the cellular source of disease-associated autoantibodies by the durability of serum titers following B cell depletion. Data from clinical trials and animal models across different autoimmune diseases may provide useful insights into the lifespan, lifestyle and fate of autoreactive plasma cells.

中文翻译：

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它的长短：观察B细胞耗竭疗法揭示的自身抗体的细胞来源。

高滴度的致病性自身抗体是许多自身免疫性疾病的标志。然而，关于疾病的关键介导者自反应性浆细胞仍然未知。我们提出了一个模型，其中前体B细胞耗竭用于体液自身免疫治疗的不同功效可以通过短期生存期与长期生存期浆细胞的致病抗体相对贡献的差异来解释。除了治疗方面的考虑外，该模型还表明我们可以通过B细胞耗竭后血清滴度的持久性来推断疾病相关自身抗体的细胞来源。来自跨不同自身免疫性疾病的临床试验和动物模型的数据可能为了解自身反应性浆细胞的寿命，生活方式和命运提供有用的见识。