Citations 2
Ahr-Foxp3-RORγt axis controls gut homing of CD4 + T cells by regulating GPR15
Xiong, Lifeng , Dean, Joseph , Fu, Zheng , Oliff, Kristen N., Bostick, John W. , Ye, Jian , Chen, Zongming E., Mühlbauer, Marcus , Zhou, Liang , Dean, Joseph W
Science Immunology | June 12, 2020 | Volume: 5 | Issue: 48 | Pages: No page available
GPR15 expression is promoted by Ahr in an evolutionarily conserved manner via cooperation with Foxp3 but inhibited by RORγt.
Dichotomous regulation of group 3 innate lymphoid cells by nongastric Helicobacter species
Bostick, John W. , Shen, Zeli , Ge, Yong, Brown, Jeffrey B. , Chen, Zong-ming E., Mohamadzadeh, Mansour , Fox, James G. , Zhou, Liang , Wang, Yetao , Ge, Yong
Proceedings of the National Academy of Sciences | November 18, 2019 | Volume: 116 | Issue: 49 | Pages: 24760-24769
Intestinal innate lymphoid cells (ILCs) contribute to the protective immunity and homeostasis of the gut, and the microbiota are critically involved in shaping ILC function. However, the role of the gut microbiota in regulating ILC development and maintenance still remains elusive. Here, we identified opposing effects on ILCs by two Helicobacter species, Helicobacter apodemus and Helicobacter typhlonius , isolated from immunocompromised mice. We demonstrated that the introduction of both Helicobacter species activated ILCs and induced gut inflammation; however, these Helicobacter species negatively regulated RORγt + group 3 ILCs (ILC3s), especially T-bet + ILC3s, and diminished their proliferative capacity. Thus, these findings underscore a previously unknown dichotomous regulation of ILC3s by Helicobacter species, and may serve as a model for further investigations to elucidate the host–microbe interactions that critically sustain the maintenance of intestinal ILC3s.