1. The transcription factor Bcl11b is specifically expressed in group 2 innate lymphoid cells and is essential for their development
- Author
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Pentao Liu, Cui Wang, Neal G. Copeland, Juexuan Wang, Daqian He, Shannon Burke, Yong Yu, Gordon Dougan, Liming Lu, Nancy A. Jenkins, Simon Clare, Song Choon Lee, and Cordelia Brandt
- Subjects
Male ,Zinc finger ,Innate immune system ,Tumor Suppressor Proteins ,BCL11B ,BCL11B Gene ,Immunology ,Innate lymphoid cell ,Brief Definitive Report ,Biology ,3. Good health ,Repressor Proteins ,Haematopoiesis ,Immune system ,Gene Expression Regulation ,Animals ,Humans ,Immunology and Allergy ,Female ,Lymphocytes ,Transcription factor - Abstract
Yu et al. demonstrate that the transcription factor Bcl11b is specifically expressed in mouse innate lymphoid progenitors committed to the ILC2 lineage and is required for their development. Bcl11b-deficient mice exhibit a complete lack of ILC2 development, which is confirmed by immune challenges with either papain treatment or influenza virus infection., Group 2 innate lymphoid cells (ILCs), or ILC2s, are a subset of recently identified ILCs, which play important roles in innate immunity by producing type 2 effector cytokines. Several transcription factors have been found to have critical functions in the development of both ILC2s and T cells. We report here that Bcl11b, a transcription factor essential in T cell lineage commitment and maintenance, is specifically expressed in progenitors committed to the ILC2 lineage and is required for ILC2 development. The Bcl11b gene is expressed in ∼28% of ILC progenitors (ILCPs; common helper innate lymphoid progenitors or ILCPs expressing either ID2 or promyelocytic leukemia zinc finger, respectively). Both in vitro and in vivo, these Bcl11b-expressing early ILCPs generate only ILC2s. Inactivation of Bcl11b causes a complete loss of ILC2 development from hematopoietic progenitors, which is confirmed upon immune challenge with either papain administration or influenza virus infection.
- Published
- 2015
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