B-1 cell development: evidence for an uncommitted immunoglobulin (Ig)M+ B cell precursor in B-1 cell differentiation.
B-1 cell development: evidence for an uncommitted immunoglobulin (Ig)M+ B cell precursor in B-1 cell differentiation.
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B-1细胞发育：B-1细胞分化中未施加的免疫球蛋白（IG）M+ B细胞前体的证据。
DOI：
10.1084/jem.187.8.1325
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发表时间：
1998-04-20
影响因子：
15.3
通讯作者：
Arnold, LW
中科院分区：
文献类型：
--
作者：
Clarke, SH;Arnold, LW
小鼠磷脂酰胆碱（PtC）特异性B细胞在正常小鼠只属于B-1亚群。对抗ptc （VH12和VH12/Vκ4）转基因（Tg）小鼠的分析表明，免疫球蛋白基因重排后发生了B-0（也称为B-2）的排斥。这预示了ptc特异性B-0细胞的产生，但随后因凋亡或分化为B-1而被消除。为了研究排除机制，在表达x连锁免疫缺陷（xid）突变的小鼠中检测了ptc特异性B细胞分化。xid小鼠缺乏功能性布鲁顿酪氨酸激酶（Btk），这是B细胞受体信号转导途径的一个组成部分，并且缺乏B-1细胞发育。我们在C57BL/ 6中找到。xid小鼠发现VH12 pre-BII细胞选择正常，ptc特异性B细胞进行适度克隆扩增。然而，抗ptc Tg/xid小鼠的脾脏ptc特异性B细胞大多数是B-0，而非非氧化小鼠的B-1。这些数据表明ptc特异性B-0细胞的产生先于预期的分离，并且Btk功能是有效分离到B-1所必需的。由于xid小鼠表现出有缺陷的B细胞分化，而不是程序性细胞死亡，这些数据与ptc特异性B-0细胞无法转化为B-1和单一B细胞谱系最为一致。
Murine phosphatidyl choline (PtC)–specific B cells in normal mice belong exclusively to the B-1 subset. Analysis of anti-PtC (VH12 and VH12/Vκ4) transgenic (Tg) mice indicates that exclusion from B-0 (also known as B-2) occurs after immunoglobulin gene rearrangement. This predicts that PtC-specific B-0 cells are generated, but subsequently eliminated by either apoptosis or differentiation to B-1. To investigate the mechanism of exclusion, PtC-specific B cell differentiation was examined in mice expressing the X-linked immunodeficiency (xid) mutation. xid mice lack functional Bruton's tyrosine kinase (Btk), a component of the B cell receptor signal transduction pathway, and are deficient in B-1 cell development. We find in C57BL/ 6.xid mice that VH12 pre-BII cell selection is normal and that PtC-specific B cells undergo modest clonal expansion. However, the majority of splenic PtC-specific B cells in anti-PtC Tg/xid mice are B-0, rather than B-1 as in their non-xid counterparts. These data indicate that PtC-specific B-0 cell generation precedes segregation as predicted, and that Btk function is required for efficient segregation to B-1. Since xid mice exhibit defective B cell differentiation, not programmed cell death, these data are most consistent with an inability of PtC-specific B-0 cells to convert to B-1 and a single B cell lineage.
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DOI：
10.1084/jem.172.1.371
发表时间：
1990-07-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Carmack CE;Shinton SA;Hayakawa K;Hardy RR
通讯作者：
Hardy RR
DOI：
10.1084/jem.157.1.202
发表时间：
1983-01-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Hayakawa K;Hardy RR;Parks DR;Herzenberg LA
通讯作者：
Herzenberg LA
DOI：
10.1073/pnas.88.24.11550
发表时间：
1991-12-01
影响因子：
11.1
作者：
HARDY, RR;HAYAKAWA, K
通讯作者：
HAYAKAWA, K
影响因子：
5.4
作者：
CLARKE, SH;MCCRAY, SK
通讯作者：
MCCRAY, SK
影响因子：
15.3
作者：
Hayakawa, K;Hardy, R R;Herzenberg, L A;Herzenberg, L A
通讯作者：
Herzenberg, L A