Glode L M, Scher I, Osborne B, Rosenstreich D L
J Immunol. 1976 Feb;116(2):454-61.
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.
C3H/HeJ小鼠的B细胞对一种内毒素（LPS K235）无反应，而该内毒素对包括密切相关的C3H/HeN品系在内的正常小鼠具有促有丝分裂作用。已对这种无反应状态的细胞基础进行了研究。C3H/HeJ小鼠的B细胞数量正常，能够对其他B细胞促有丝分裂原，如多聚肌苷酸（Poly I）产生正常反应。添加正常巨噬细胞或脾细胞无法恢复正常反应。此外，C3H/HeJ品系的巨噬细胞和脾细胞均不会抑制正常C3H/HeN脾细胞。最后，通过去除巨噬细胞或T细胞而富集B细胞的脾细胞对LPS的反应性也表现出相同的差异。这些结果表明，LPS无反应性是B细胞自身的缺陷，而非由于抑制细胞或辅助细胞的缺失。当将LPS添加到经Poly I刺激的培养物中时，正常C3H/HeN脾细胞的反应会进一步增强。然而，LPS会导致C3H/HeJ脾细胞的Poly I反应受到剂量依赖性抑制。这种抑制取决于将LPS添加到经Poly I刺激的培养物中的时间。这些数据被解释为表明LPS与C3H/HeJ B细胞膜的结合导致其失活或受到抑制，而这就是该小鼠品系中LPS无反应性的基础。
