期刊
ANNUAL REVIEW OF IMMUNOLOGY, VOL 32
卷 32, 期 -, 页码 283-321出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-immunol-032712-100024
关键词
lymphocyte development; gene regulatory network; transcription factors; Notch
类别
资金
- NCI NIH HHS [R01 CA090233, RC2 CA148278, CA90233, CA148278] Funding Source: Medline
- NHLBI NIH HHS [HL89123, R33 HL089123] Funding Source: Medline
- NIAID NIH HHS [R01 AI095943, AI95943, R01 AI083514, R56 AI083514, AI83514] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA090233, RC2CA148278] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R33HL089123] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R56AI083514, R01AI083514, R01AI095943] Funding Source: NIH RePORTER
T and B cells share a common somatic gene rearrangement mechanism for assembling the genes that code for their antigen receptors; they also have developmental pathways with many parallels. Shared usage of basic helix-loop-helix E proteins as transcriptional drivers underlies these common features. However, the transcription factor networks in which these E proteins are embedded are different both in membership and in architecture for T and B cell gene regulatory programs. These differences permit lineage commitment decisions to be made in different hierarchical orders. Furthermore, in contrast to B cell gene networks, the T cell gene network architecture for effector differentiation is sufficiently modular so that E protein inputs can be removed. Complete T cell-like effector differentiation can proceed without T cell receptor rearrangement or selection when E proteins are neutralized, yielding natural killer and other innate lymphoid cells.
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