NF-kappaB2-p100在调节性T细胞稳态和激活中的作用。,Scientific Reports - X-MOL

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NF-kappaB2-p100在调节性T细胞稳态和激活中的作用。
Scientific Reports ( IF 3.8 ) Pub Date : 2019-09-25 , DOI: 10.1038/s41598-019-50454-z
Atika Dhar ₁ , Meenakshi Chawla ₁ , Somdeb Chattopadhyay ₁ , Neelam Oswal ₁ , Danish Umar ₁ , Suman Gupta ₁ , Vineeta Bal ₁ , Satyajit Rath ₁ , Anna George ₁ , G Aneeshkumar Arimbasseri ₁ , Soumen Basak ₁

Affiliation

核因子-κB（NF-κB）途径的免疫学作用是通过免疫反应中的典型成分以及免疫器官发生和体内稳态中的非经典成分介导的，尽管这两个成分都具有相互干扰的能力。调节性CD4 T细胞（Tregs）具有稳态功能，代表了这两个NF-κB组分有趣的潜在交汇点。我们显示，在非规范的NF-κB成分基因Nfkb2（p100）中缺乏的小鼠具有正常的胸腺发育和Tregs的抑制功能。然而，它们具有提高的外周“效应表型” Tregs（eTregs）的频率。在野生型（WT）和Nfkb2-/-小鼠的双亲嵌合体中，Nfkb2-/-基因型在Tregs中过度表达，eTregs的相对突出度进一步增加。与eTregs的独特特性一致，Nfkb2-/-基因型在双亲嵌合体的肝外淋巴组织中的Tregs中更为突出。Nfkb2-/-Tregs在体内也显示出更大的存活，激活和增殖。这些Nfkb2-/-Tregs显示出较高的核NF-κB活性，主要由含RelB的二聚体组成，与WT Tregs中含cRel和RelA的二聚体的突出相反。由于p100是RelB激活的抑制剂，也是p52在RelB核活性中裂解的参与者，因此我们测试了WT和Relb-/-小鼠的双亲嵌合体，并发现这些小鼠中Relb-/-Treg和eTreg的正常频率嵌合小鼠。我们的发现证实并扩展了最近的数据，并表明p100通常会抑制RelB介导的Treg激活，而在没有p100的情况下，

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Role of NF-kappaB2-p100 in regulatory T cell homeostasis and activation.

The immunological roles of the nuclear factor-kappaB (NF-κB) pathway are mediated via the canonical components in immune responses and via non-canonical components in immune organogenesis and homeostasis, although the two components are capable of crosstalk. Regulatory CD4 T cells (Tregs) are homeostatically functional and represent an interesting potential meeting point of these two NF-κB components. We show that mice deficient in the non-canonical NF-κB component gene Nfkb2 (p100) had normal thymic development and suppressive function of Tregs. However, they had enhanced frequencies of peripheral 'effector-phenotype' Tregs (eTregs). In bi-parental chimeras of wild-type (WT) and Nfkb2-/- mice, the Nfkb2-/- genotype was over-represented in Tregs, with a further increase in the relative prominence of eTregs. Consistent with distinct properties of eTregs, the Nfkb2-/- genotype was more prominent in Tregs in extra-lymphoid tissues such as liver in the bi-parental chimeras. The Nfkb2-/- Tregs also displayed greater survival, activation and proliferation in vivo. These Nfkb2-/- Tregs showed higher nuclear NF-κB activity mainly comprising of RelB-containing dimers, in contrast to the prominence of cRel- and RelA-containing dimers in WT Tregs. Since p100 is an inhibitor of RelB activation as well as a participant as cleaved p52 in RelB nuclear activity, we tested bi-parental chimeras of WT and Relb-/- mice, and found normal frequencies of Relb-/- Tregs and eTregs in these chimeric mice. Our findings confirm and extend recent data, and indicate that p100 normally restrains RelB-mediated Treg activation, and in the absence of p100, p50-RelB dimers can contribute to Treg activation.

更新日期：2019-09-26

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