期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 201, 期 8, 页码 1197-1203出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20050158
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资金
- NCI NIH HHS [R01 CA098129, R01 CA98129] Funding Source: Medline
- NIAID NIH HHS [T32 AI052077, T32 AI52077, R01 AI056123] Funding Source: Medline
Cytokine receptor signals have been suggested to stimulate cell differentiation during hemato/lymphopoiesis. Such action, however, has not been clearly demonstrated. Here, we show that adult B cell development in IL-7(-/-) and IL-7R alpha(-/-) mice is arrested at the pre-pro-B cell stage due to insufficient expression of the B cell-specific transcription factor EBF and its target genes, which form a transcription factor network in determining B lineage specification. EBF expression is restored in IL-7(-/-) pre-pro-B cells upon IL-7 stimulation or in IL-7R alpha(-/-) pre-pro-B cells by activation of STAT5, a major signaling molecule downstream of the IL-7R signaling pathway. Furthermore, enforced EBF expression partially rescues B cell development in IL-7R alpha(-/-) mice. Thus, IL-7 receptor signaling is a participant in the formation of the transcription factor network during B lymphopoiesis by up-regulating EBF, allowing stage transition from the pre-pro-B to further maturational stages.
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