Neonatally induced inactivation of the vascular cell adhesion molecule 1 gene impairs B cell localization and T cell-dependent humoral immune response.
Neonatally induced inactivation of the vascular cell adhesion molecule 1 gene impairs B cell localization and T cell-dependent humoral immune response.
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DOI：
10.1084/jem.193.6.755
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发表时间：
2001-03-19
期刊：
影响因子：
--
通讯作者：
Wagner N
中科院分区：
文献类型：
--
作者：
Leuker CE;Labow M;Müller W;Wagner N
血管细胞粘附分子（VCAM）-1是一种膜结合的细胞粘合剂分子，可介导造血祖细胞和骨髓（BM）中的基质细胞之间的粘合剂相互作用，以及白细胞和内皮细胞和内皮细胞和树突状细胞 - 缺乏小鼠胚胎死亡，有条件的VCAM-1突变体是生成该广告分子的体内功能的。干扰素诱导的Cre-loxP介导的VCAM-1基因的缺失在大多数组织中有效地消融了VCAM-1的表达，例如BM，淋巴机构和肺部，但在大脑中却没有导致BM中未成熟的B细胞的降低，并在外周血中增加这些细胞，但在淋巴机器人中没有降低。静脉注射后BM中出现的成熟B细胞还减少了对T细胞依赖性抗原的体外响应。 。
Vascular cellular adhesion molecule (VCAM)-1 is a membrane-bound cellular adhesion molecule that mediates adhesive interactions between hematopoietic progenitor cells and stromal cells in the bone marrow (BM) and between leukocytes and endothelial as well as dendritic cells. Since VCAM-1–deficient mice die embryonically, conditional VCAM-1 mutant mice were generated to analyze the in vivo function of this adhesion molecule. Here we show that interferon-induced Cre-loxP–mediated deletion of the VCAM-1 gene after birth efficiently ablates expression of VCAM-1 in most tissues like, for example, BM, lymphoid organs, and lung, but not in brain. Induced VCAM-1 deficiency leads to a reduction of immature B cells in the BM and to an increase of these cells in peripheral blood but not in lymphoid organs. Mature recirculating B cells are reduced in the BM. In a migration assay, the number of mature B cells that appears in the BM after intravenous injection is decreased. In addition, the humoral immune response to a T cell–dependent antigen is impaired. VCAM-1 serves an important role for B cell localization and the T cell–dependent humoral immune response.
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DOI：
10.1084/jem.179.4.1391
发表时间：
1994-04-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Hahne M;Wenger RH;Vestweber D;Nielsen PJ
通讯作者：
Nielsen PJ
影响因子：
4.1
作者：
KAMATA, T;PUZON, W;TAKADA, Y
通讯作者：
TAKADA, Y
影响因子：
6.5
作者：
Craddock, CF;Nakamoto, B;Papayannopoulou, T
通讯作者：
Papayannopoulou, T
影响因子：
20.3
作者：
Brasel, K;McKenna, HJ;Lyman, SD
通讯作者：
Lyman, SD
影响因子：
4.4
作者：
Forster, I;Vieira, P;Rajewsky, K
通讯作者：
Rajewsky, K