脂多糖激活B细胞。诱导有丝分裂和抗体产生的不同途径。
B-cell activation by lipopolysaccharide. Distinct pathways for induction of mitosis and antibody production.
作者信息
Hoffmann M K, Galanos C, Koenig S, Oettgen H F
出版信息
J Exp Med. 1977 Dec 1;146(6):1640-7. doi: 10.1084/jem.146.6.1640.
Abstract
The role played by macrophages in two effects of lipopolysaccharide (LPS) on the immune system of the mouse-substitution for helper T cells and induction of B-cell mitosis-has been investigated. C3H/HeJ mice are unresponsive and do not produce (as other strains do) antibody to 2,4,6-trinitrophenol (TNP) conjugated with autologous mouse erythrocytes (MRBC-TNP) in the presence of LPS. We found that C3H/HeJ spleen cells produce antibody to MRBC-TNP when (a) LPS and macrophages from LPS-responsive C3HeB/FeJ mice or (b) tumor necrosis serum ([TNS] induced by LPS in responsive mice) are added. The mitotic response was not restored. The findings suggest that adjuvanticity and mitogenicity represent distinct pathways of B-cell activation by LPS, subject to different regulatory mechanisms.
摘要
巨噬细胞在脂多糖（LPS）对小鼠免疫系统的两种作用（替代辅助性T细胞以及诱导B细胞有丝分裂）中所起的作用已得到研究。C3H/HeJ小鼠无反应，在LPS存在的情况下，不会（像其他品系那样）产生针对与自体小鼠红细胞结合的2,4,6-三硝基苯酚（TNP）的抗体（MRBC-TNP）。我们发现，当添加（a）LPS和来自对LPS有反应的C3HeB/FeJ小鼠的巨噬细胞或（b）肿瘤坏死血清（[TNS]，由LPS在有反应的小鼠中诱导产生）时，C3H/HeJ脾细胞会产生针对MRBC-TNP的抗体。有丝分裂反应未恢复。这些发现表明，佐剂性和促有丝分裂性代表了LPS激活B细胞的不同途径，受不同的调节机制控制。
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