Cellular mechanism of endotoxin unresponsiveness in C3H/HeJ mice.
Cellular mechanism of endotoxin unresponsiveness in C3H/HeJ mice.
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C3H/HeJ 小鼠内毒素无反应的细胞机制。
DOI：
10.4049/jimmunol.116.2.454
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发表时间：
1976
影响因子：
4.4
通讯作者：
D. Rosenstreich
中科院分区：
文献类型：
--
作者：
L. Glodé;I. Scher;B. Osborne;D. Rosenstreich
来自C3H/HeJ小鼠的B细胞不能对内毒素(LPSK235)做出反应，内毒素对正常小鼠(包括近缘关系密切的C3H/HEN品系)是有丝分裂的。这种无反应状态的细胞基础已经被研究过了。C3H/HeJ小鼠的B细胞数量正常，能够对其他B细胞有丝分裂原正常反应，如多聚肌苷酸(Poly I)。加入正常的巨噬细胞或脾细胞不能重建正常的反应。此外，C3H/HeJ株的巨噬细胞和脾细胞都不能抑制正常的C3H/HEN脾细胞。最后，通过去除巨噬细胞或T细胞来浓缩B细胞的脾细胞在对内毒素的反应性方面表现出相同的差异。这些结果表明，内毒素无反应性是B细胞本身的缺陷，而不是由于抑制细胞或辅助细胞的缺失。当LPS加入到Poly I刺激的培养物中时，正常C3H/HEN脾细胞的反应有额外的增强。然而，内毒素对C3H/HeJ脾细胞的Poly I反应具有剂量依赖性抑制作用。这种抑制作用依赖于在Poly-I刺激的培养中加入内毒素的时间。这些数据被解释为表明内毒素与C3H/HeJ B细胞膜的结合导致其失活或抑制，这是该小鼠品系内毒素无反应的基础。
B cells from C3H/HeJ mice fail to respond to an endotoxin (LPS K235) which is mitogenic for normal mice including the closely related C3H/HeN strain. The cellular basis for this unresponsive state has been investigated. The C3H/HeJ mice have normal numbers of B cells, which are capable of normal responses to other B cell mitogens, such as polyinosinic acid (Poly I). Addition of normal macrophages or spleen cells fails to reconstitute the normal response. Furthermore, neither macrophages nor spleen cells from the C3H/HeJ strain suppress the normal C3H/HeN spleen cells. Finally, spleen cells enriched for B cells by the removal of macrophages or T cells demonstrate the same differences in responsiveness to LPS. These results indicate that LPS unresponsiveness is a defect of the B cell itself and not due to suppressor cells or the absence of helper cells. When LPS is added to Poly I-stimulated cultures, there is additional enhancement of the response of normal C3H/HeN spleen cells. However, LPS causes a dose-dependent suppression of the Poly I response of C3H/HeJ spleen cells. This suppression is dependent on the time of addition of LPS to the Poly I-stimulated cultures. These data are interpreted as indicating that the binding of LPS to the membrane of C3H/HeJ B cells results in their inactivation or suppression, and that this is the basis of LPS unresponsiveness in this mouse strain.