RelB, a member of the NF-κB family, plays a critical role in the development of T cells. However, the role of RelB in Foxp3+ regulatory T cells (Tregs) remains controversial. Using a bone marrow chimeric mouse model, we demonstrated that the expansion of Foxp3+ Tregs in vivo could be mediated by extrinsic mechanisms. RelB plays an important role in inhibiting the homeostatic proliferation of Tregs, but not their survival. Even with the heightened expansion, RelB−/− Treg cells displayed normal suppressive function in vitro. Among the expanded populations of Treg cells, most were nTreg cells; however, the population of iTregs did not increase. Mechanistically, RelB seems to regulate Treg proliferation independently of the signal transducer and activator of transcription 5 (STAT5) pathway. These data suggest that RelB regulates Treg proliferation independently of the STAT5 pathway, but does not alter the function of Tregs. Further studies are warranted to uncover such mechanisms.

中文翻译：

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RelB调节稳态增殖，但不调节Treg的功能。

RelB是NF-κB家族的成员，在T细胞的发育中起关键作用。但是，RelB在Foxp3 +调节性T细胞（Tregs）中的作用仍存在争议。使用骨髓嵌合体小鼠模型，我们证明了Foxp3 + Tregs在体内的扩增可能是由外在机制介导的。RelB在抑制Treg的稳态增殖中起着重要作用，但在抑制其存活方面却起着重要的作用。即使扩展增加，RelB-/-Treg细胞在体外仍显示正常的抑制功能。在扩增的Treg细胞群中，大多数是nTreg细胞；但是，iTregs的数量并未增加。从机理上讲，RelB似乎独立于信号转导子和转录激活子5（STAT5）途径调节Treg增殖。这些数据表明RelB独立于STAT5途径调节Treg的增殖，但不会改变Treg的功能。有必要做进一步的研究来揭示这种机制。