Systemic lupus erythematosus (SLE) is a highly heterogeneous autoimmune disease characterised by the production of pathogenic autoantibodies against nuclear self-antigens. The anti-inflammatory and tolerogenic cytokine Interleukin-10 appears to play a paradoxical pathogenic role in SLE and is therefore currently therapeutically targeted in clinical trials. It is generally assumed that the pathogenic effect of IL-10 in SLE is due to its growth and differentiation factor activity on autoreactive B-cells, but effects on other cells might also play a role. To date, a unique cellular source of pathogenic IL-10 in SLE has not been identified. In this review, we focus on the contribution of different CD4⁺T-cell subsets to IL-10 and autoantibody production in SLE. In particular, we discuss that IL-10 produced by different subsets of adaptive regulatory T-cells, follicular helper T-cells and extra-follicular B-helper T-cells is likely to have different effects on autoreactive B-cell responses. A better understanding of the role of IL-10 in B-cell responses and lupus would allow to identify the most promising therapies for individual SLE patients in the future.

系统性红斑狼疮（SLE）是一种高度异质性自身免疫疾病，其特征是产生针对核自身抗原的致病性自身抗体。抗炎和耐受性细胞因子白细胞介素10在SLE中似乎起着悖论的致病作用，因此目前在临床试验中被靶向治疗。通常认为IL-10在SLE中的致病作用是由于其对自身反应性B细胞的生长和分化因子活性，但对其他细胞的作用也可能起作用。迄今为止，尚未鉴定出SLE中病原性IL-10的独特细胞来源。在这篇评论中，我们重点介绍不同CD4 ⁺SLE中IL-10的T细胞亚群和自身抗体的产生。特别是，我们讨论了由适应性调节性T细胞，滤泡性辅助性T细胞和滤泡性辅助性T细胞的不同子集产生的IL-10可能会对自身反应性B细胞反应产生不同的影响。更好地了解IL-10在B细胞反应和狼疮中的作用将有助于确定将来针对单个SLE患者的最有希望的疗法。