期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 202, 期 10, 页码 1411-1422出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20051089
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资金
- NCI NIH HHS [R01 CA089590, R01 CA89590-01] Funding Source: Medline
- NINDS NIH HHS [R01 NS43881-01, R01 NS043881] Funding Source: Medline
In this paper, we describe the unexpected outgrowth of B lineage cells from PU.1(-/-) fetal liver cultures. The cells express all early B cell genes tested, including the putative PU.1 target genes IL-7R and EBF but not B220, and can produce immunoglobulin M. However, we observed a delay in the PU.1(-/-) B cell outgrowth and reduced precursor frequencies, indicating that although PU.1 is not strictly required for B cell commitment, it facilitates B cell development. We also ablated PU.1 in CD19-expressing B lineage cells in vivo, using a Cre-lox approach that allows them to be tracked. PU.1 excision resulted in a shift from B-2 cells to B-1-like cells, which dramatically increased with the age of the mice. Our data indicate that this shift is predominantly caused by a B-2 to B-1 cell reprogramming. Furthermore, we found that B-2 cells express substantially more PU.1 than B-1 cells, which is consistent with the idea that maintenance of the B-2 cell phenotype requires relatively high levels of PU.1, but B-1 cells require little.
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