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Xiao He
Researcher at University of Utah
Publications - 28
Citations - 979
Xiao He is an academic researcher from University of Utah. The author has contributed to research in topics: T cell & CD8. The author has an hindex of 12, co-authored 28 publications receiving 844 citations. Previous affiliations of Xiao He include Fox Chase Cancer Center & Washington University in St. Louis.
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Journal ArticleDOI
The zinc finger transcription factor Th-POK regulates CD4 versus CD8 T-cell lineage commitment
Xiao He,Xi He,Vibhuti P. Dave,Yi Zhang,Xiang Hua,Emmanuelle Nicolas,Weihong Xu,Bruce A. Roe,Dietmar J. Kappes +8 more
TL;DR: It is shown that a point mutation in the zinc finger transcription factor Th-POK (T-helper-inducing POZ/Krüppel-like factor) is responsible for redirection of class-II-restricted thymocytes to the CD8 lineage in HD mice, indicating that Th- POK is a master regulator of lineage commitment.
Journal ArticleDOI
CD4-CD8 Lineage Commitment Is Regulated by a Silencer Element at the ThPOK Transcription-Factor Locus
Xi He,Kyewon Park,Kyewon Park,Haitao Wang,Xiao He,Yi Zhang,Xiang Hua,Yi Li,Dietmar J. Kappes +8 more
TL;DR: A silencer-dependent model of lineage choice is proposed, whereby inactivation of the DRE silencer by a strong TCR signal leads to CD4 commitment, whereas continued silencer activity leads toCD8 commitment.
Journal ArticleDOI
CD4-CD8 lineage commitment: an inside view.
Dietmar J. Kappes,Xiao He,Xi He +2 more
TL;DR: The mechanism of CD4-CD8 lineage commitment, which ensures the correlation between T cell receptor specificity and adoption of the T killer or T helper phenotype, has long been the subject of intense debate as mentioned in this paper.
Journal Article
Late induction of CREB/ATF binding and a concomitant increase in cAMP levels in T and B lymphocytes stimulated via the antigen receptor.
TL;DR: Results suggest that recruitment of CREB and ATF2 to the promoter of genes is tightly regulated during activation of T and B lymphocytes and implicate a cross-talk of cAMP and non-cAMP pathways in the regulation of transcriptional processes at late stages of activation in T andB lymphocytes stimulated via the Ag receptor.
Journal ArticleDOI
Depletion of PD-1-positive cells ameliorates autoimmune disease.
Peng Zhao,Peng Wang,Shuyun Dong,Zemin Zhou,Yanguang Cao,Hideo Yagita,Xiao He,Song Guo Zheng,Simon J. Fisher,Robert S. Fujinami,Mingnan Chen +10 more
TL;DR: An immunotoxin incorporating an anti-programmed-cell-death-protein-1 (PD-1) single-chain variable fragment selectively eliminates PD-1-expressing cells, and suppresses autoimmunity while preserving adaptive immunity in mouse models of autoimmune disease.