Rosenstreich D L, Vogel S N, Jacques A, Wahl L M, Scher I, Mergenhagen S E
J Immunol. 1978 Aug;121(2):685-90.
The in vitro sensitivity of B lymphocytes and macrophages derived from (CBA/N X DBA/2N) F1 male mice, which carry an X-linked recessive gene that produces defective B cell maturation, was compared to phenotypically normal F1 female mice. B lymphocytes of F1 males exhibit an abnormal mitogenic response to LPS in serum-free culture conditions, which is partially reversed in the presence of serum. In contrast, both resident and thioglycollate-induced peritoneal macrophages of F1 male mice respond normally to LPS. In response to LPS in vitro, F1 male macrophages produce the monokine, lymphocyte-activating factor (LAF) and release prostaglandins. Furthermore, F1 male macrophages are sensitive to the lethal effects of LPS. Therefore, the defective CBA/N gene appears to be expressed only in B lymphocytes and not in macrophages. Since F1 male mice are normally sensitive to the lethal and adjuvant effects of LPS in vivo, these findings suggest that a mature B lymphocyte population is not required for these effects and support the role of the macrophage in the mediation of LPS-induced lethality and adjuvanticity.
将携带产生缺陷性B细胞成熟的X连锁隐性基因的（CBA/N×DBA/2N）F1雄性小鼠衍生的B淋巴细胞和巨噬细胞的体外敏感性，与表型正常的F1雌性小鼠进行了比较。F1雄性小鼠的B淋巴细胞在无血清培养条件下对LPS表现出异常的促有丝分裂反应，在有血清存在时该反应会部分逆转。相比之下，F1雄性小鼠的驻留型和巯基乙酸诱导的腹腔巨噬细胞对LPS的反应正常。在体外对LPS的反应中，F1雄性巨噬细胞产生单核因子、淋巴细胞激活因子（LAF）并释放前列腺素。此外，F1雄性巨噬细胞对LPS的致死作用敏感。因此，有缺陷的CBA/N基因似乎仅在B淋巴细胞中表达，而不在巨噬细胞中表达。由于F1雄性小鼠在体内通常对LPS的致死和佐剂作用敏感 , 这些发现表明这些作用不需要成熟的B淋巴细胞群体，并支持巨噬细胞在介导LPS诱导的致死性和佐剂性中的作用。
