2篇
您的检索式：作者名="Preston R.Arnold"
|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Transcriptional and epigenetic regulation of immune tolerance:roles of the NF-κB family members显示文摘Immune tolerance is a highly regulated state and involves diverse mechanisms.Central to the induction of tolerance is the targeted modulation of T-cell activities(both effector and regulatory),in which transcription factors play a significant role.The nuclear factor kappa-B(NF-κB)family is a family of transcription factors that not only are critically involved in diverse T-cell responses but also are regulated by many mechanisms to maintain tolerance and T-cell homeostasis.NF-κB,as a transcription factor,has been extensively studied in recent decades,and the molecular mechanisms that regulate NF-κB activities have been well documented.However,recent studies have revealed exciting new roles for NF-κB;in addition to its transcriptional activity,NF-κB can also activate diverse epigenetic mechanisms that mediate extensive chromatin remodeling of target genes to regulate T-cell activities.In this review article,we highlight recent discoveries and emerging opportunities in targeting NF-κB family members as well as their associated chromatin modifiers in the induction of immune tolerance and in the clinical treatment of immune diseases. | Lei Zhang Xiang Xiao Preston R.Arnold Xian C.Li | 2019 | Cellular & Molecular Immunology2019，16，4： | 5 |
| 2 | The transcription factor RelB restrains group 2 innate lymphoid cells and type 2 immune pathology in vivo显示文摘The exact relationships between group 2 innate lymphoid cells(ILC2s)and Th2 cells in type 2 pathology,as well as the mechanisms that restrain the responses of these cells,remain poorly defined.Here we examined the roles of ILC2s and Th2 cells in type 2 lung pathology in vivo using germline and conditional fie/b-deficient mice.We found that mice with germline deletion of Relb^(-/-)spontaneously developed prominent type 2 pathology in the lung,which contrasted sharply with mice with T-cell-specific Relb deletion(Relb^(f/f)Cd4-Cre),which were healthy with no observed autoimmune pathology.We also found that in contrast to wild-type B6 mice,Rel6-defident mice showed markedly expanded ILC2s but not ILC1s or ILC3s.Moreover,adoptive transfer of naive CD4^(+)T cells into Rag1^(-/-)Relb^(-/-)hosts induced prominent type 2 lung pathology,which was inhibited by depletion of ILC2s.Mechanistically,we showed that Relb deletion led to enhanced expression of Bcl11b,a key transcription factor for ILC2s.We concluded that RelB plays a critical role in restraining ILC2s,primarily by suppressing Bcl11b activity,and consequently inhibits type 2 lung pathology in vivo. | Lei Zhang Yuanlin Ying Shuqiu Chen Preston R.Arnold Fafa Tian Laurie J.Minze Xiang Xiao Xian C.Li | 2021 | Cellular & Molecular Immunology2021，18，1： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员