Phenotypic changes of bone marrow-derived mast cells after intraperitoneal transfer into W/Wv mice that are genetically deficient in mast cells.
Phenotypic changes of bone marrow-derived mast cells after intraperitoneal transfer into W/Wv mice that are genetically deficient in mast cells.
复制标题
腹膜内转移到肥大细胞中遗传缺陷的W/WV小鼠中后，骨髓衍生的肥大细胞的表型变化。
DOI：
10.1084/jem.165.3.615
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发表时间：
1987-03-01
影响因子：
15.3
通讯作者：
KITAMURA, Y
中科院分区：
文献类型：
--
作者：
OTSU, K;NAKANO, T;KANAKURA, Y;ASAI, H;KATZ, HR;AUSTEN, KF;STEVENS, RL;GALLI, SJ;KITAMURA, Y
小鼠 IL-3 依赖性骨髓培养源性肥大细胞 (BMMC) 在过继转移至肥大细胞缺陷小鼠后在体内生成浆膜肥大细胞 (SMC) 的能力已通过化学和免疫化学标准进行了定义。 BMMC 在含有 PWM/脾细胞条件培养基的培养基中从 WBB6F1-+/+ 小鼠祖细胞分化和生长，合成了约 350,000 Mr 蛋白酶抗性蛋白多糖，其含有约 55,000 Mr 糖胺聚糖（通过凝胶过滤确定）。与细胞相关的 BMMC 蛋白聚糖结合的糖胺聚糖中大约 85% 是硫酸软骨素，这是基于它们对软骨素酶 ABC 消化的敏感性；软骨素酶 ABC 生成的不饱和二糖的 HPLC 显示这些糖胺聚糖是硫酸软骨素 E。根据肝素酶和亚硝酸降解测定，与 BMMC 蛋白聚糖结合的糖胺聚糖中大约 10% 是肝素。相比之下，腹腔注射BMMC 15周后，从先天性肥大细胞缺陷型WBB6F1-W/Wv小鼠的腹膜腔中回收的肥大细胞合成了约650,000 Mr蛋白酶抗性蛋白聚糖，其中含有约105,000 Mr的约80%肝素糖胺聚糖。因此，在过继转移后，先前的SMC 肥大细胞缺陷小鼠与从正常 WBB6F1-+/+ 小鼠中恢复的小鼠相似，这些小鼠显示合成约 600,000 个 Mr 蛋白聚糖，其中含有约 115,000 个 Mr 蛋白聚糖的约 80% 肝素糖胺聚糖。通过使用 B1.1 大鼠单克隆抗体（一种识别 表位位于中性糖鞘脂球五糖神经酰胺上），大约 5% 的 BMMC 可检测到与抗体结合，而在 BMMC 过继转移后 15 周从肥大细胞缺陷小鼠中收获的大约 72% 的 SMC 呈 B1.1 阳性；来自 WBB6F1-+/+ 小鼠的约 82% 的 SMC 与抗体结合。这些生化和免疫化学数据与之前的过继转移研究的结果一致，这些研究主要根据形态学和组织化学标准来表征肥大细胞。因此，体外发育的IL-3依赖性BMMC，类似于粘膜肥大细胞的细胞，可以在体内产生表达结缔组织肥大细胞表型特征的SMC。
The ability of mouse IL-3-dependent, bone marrow culture-derived mast cells (BMMC) to generate serosal mast cells (SMC) in vivo after adoptive transfer to mast cell-deficient mice has been defined by chemical and immunochemical criteria. BMMC differentiated and grown from WBB6F1-+/+ mouse progenitor cells in medium containing PWM/splenocyte-conditioned medium synthesized a approximately 350,000 Mr protease-resistant proteoglycan bearing approximately 55,000 Mr glycosaminoglycans, as defined by gel filtration of each. Approximately 85% of the glycosaminoglycans bound to the cell-associated BMMC proteoglycans were chondroitin sulfates based upon their susceptibility to chondroitinase ABC digestion; HPLC of the chondroitinase ABC- generated unsaturated disaccharides revealed these glycosaminoglycans to be chondroitin sulfate E. As determined by heparinase and nitrous acid degradations, approximately 10% of the glycosaminoglycans bound to BMMC proteoglycans were heparin. In contrast, mast cells recovered from the peritoneal cavity of congenitally mast cell-deficient WBB6F1-W/Wv mice 15 wk after intraperitoneal injection of BMMC synthesized approximately 650,000 Mr protease-resistant proteoglycans that contained approximately 80% heparin glycosaminoglycans of approximately 105,000 Mr. Thus, after adoptive transfer, the SMC of the previously mast cell-deficient mice were like those recovered from the normal WBB6F1-+/+ mice that were shown to synthesize approximately 600,000 Mr proteoglycans that contained approximately 80% heparin glycosaminoglycans of approximately 115,000 Mr. As assessed by indirect immunofluorescence staining and flow cytometry using the B1.1 rat mAb (an antibody that recognizes an epitope located on the neutral glycosphingolipid globopentaosylceramide), approximately 5% of BMMC bound the antibody detectably, whereas approximately 72% of the SMC that were harvested from mast cell-deficient mice 15 wk after adoptive transfer of BMMC were B1.1-positive; approximately 82% of SMC from WBB6F1-+/+ mice bound the antibody. These biochemical and immunochemical data are consistent with the results of previous adoptive transfer studies that characterized mast cells primarily on the basis of morphologic and histochemical criteria. Thus, IL-3- dependent BMMC developed in vitro, cells that resemble mucosal mast cells, can give rise in vivo to SMC that express phenotypic characteristics of connective tissue mast cells.
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影响因子：
7.8
作者：
GALLI, SJ;DVORAK, AM;DVORAK, HF
通讯作者：
DVORAK, HF
影响因子：
56.9
作者：
NAGAO, K;YOKORO, K;AARONSON, SA
通讯作者：
AARONSON, SA
影响因子：
64.8
作者：
NABEL, G;GALLI, SJ;CANTOR, H
通讯作者：
CANTOR, H
影响因子：
64.8
作者：
RUITENBER, EJ;ELGERSMA, A
通讯作者：
ELGERSMA, A
DOI：
10.1016/0304-4165(79)90387-8
发表时间：
1979-01-01
期刊：
BIOCHIMICA ET BIOPHYSICA ACTA
影响因子：
--
作者：
HANDLEY, CJ;LOWTHER, DA
通讯作者：
LOWTHER, DA