Paeng N, Kido N, Kato Y, Sugiyama T, Koide N, Naruse M, Jiang G Z, Lwin T, Yoshida T, Yokochi T
Department of Microbiology and Immunology, Aichi Medical University, Nagakute, Japan.
Infect Immun. 1997 Jan;65(1):122-6. doi: 10.1128/iai.65.1.122-126.1997.
Intraperitoneal administration of lipopolysaccharide to mice induced a marked reduction of CD5+ B cells in the peritoneal cavity. The reduction was not induced by intravenous, subcutaneous, or oral administration of lipopolysaccharide. The reduction continued for about 10 days after the injection, and the CD5+ B-cell count recovered to the normal state about 14 days after the injection. The reduction of peritoneal CD5+ B cells might be caused by apoptotic cell death. Injection of lipopolysaccharide did not result in production of antibody to lipopolysaccharide. On the other hand, intraperitoneal injection of heat-killed bacteria did not induce a reduction of peritoneal CD5+ B cells and elicited the definite production of antibody to lipopolysaccharide.
给小鼠腹腔注射脂多糖可导致腹腔内CD5⁺ B细胞显著减少。静脉注射、皮下注射或口服脂多糖不会引发这种减少。注射后这种减少持续约10天，注射后约14天CD5⁺ B细胞计数恢复到正常状态。腹腔CD5⁺ B细胞的减少可能是由凋亡性细胞死亡引起的。注射脂多糖不会导致产生抗脂多糖抗体。另一方面，腹腔注射热灭活细菌不会诱导腹腔CD5⁺ B细胞减少，反而会引发抗脂多糖抗体的明确产生。
