| Autor: |
Zhang L; Immunobiology and Transplant Science Center, and Department of Surgery, Houston Methodist Hospital, Texas Medical Center, Houston, Texas, USA.; Department of Neurology, Xiangya Hospital, Central South University, Changsha, China., Ying Y; Immunobiology and Transplant Science Center, and Department of Surgery, Houston Methodist Hospital, Texas Medical Center, Houston, Texas, USA., Chen S; Immunobiology and Transplant Science Center, and Department of Surgery, Houston Methodist Hospital, Texas Medical Center, Houston, Texas, USA.; Department of Urology, Southeast University Zhongda Hospital, Nanjing, China., Arnold PR; Immunobiology and Transplant Science Center, and Department of Surgery, Houston Methodist Hospital, Texas Medical Center, Houston, Texas, USA., Tian F; Department of Neurology, Xiangya Hospital, Central South University, Changsha, China., Minze LJ, Xiao X; Immunobiology and Transplant Science Center, and Department of Surgery, Houston Methodist Hospital, Texas Medical Center, Houston, Texas, USA., Li XC; Immunobiology and Transplant Science Center, and Department of Surgery, Houston Methodist Hospital, Texas Medical Center, Houston, Texas, USA. xcli@houstonmethodist.org.; Department of Surgery, Weill Cornell Medical College of Cornell University, New York, NY, USA. xcli@houstonmethodist.org. |
| Abstrakt: |
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 Relb-deficient mice. We found that mice with germline deletion of Relb (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, Relb-deficient 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. |
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