Choi Y S
Alton Ochsner Medical Foundation, Laboratory of Cellular Immunology, New Orleans, LA 70121, USA.
Immunol Res. 1997;16(2):161-74. doi: 10.1007/BF02786360.
An in vitro experimental model was developed to characterize the cellular and molecular factors that regulate germinal center (GC)-B-cell differentiation and apoptosis. In the culture system that sustains the GC-B-cell survival, CD40L stimulation is essential for GC-B-cell proliferation and differentiation in the presence of 1L-2, IL-4, and IL-10. IL-2 and Il-4 promote proliferation of GC-B-cells, whereas IL-10 is required for generation of plasma cells. Generation of memory B cells requires CD40L, IL-2, IL-4, but not IL-10. There are two mechanisms that cause apoptosis. In the early stage, spontaneous apoptosis occurs in the absence of CD40 stimulation. Following CD40L stimulation, Fas-mediated apoptosis operates to eliminate GC-B-cells, unless activated GC-B-cells encounter a second signal via B-cell Ig receptors. Physiological significance of these findings is discussed.
建立了一种体外实验模型，以表征调节生发中心（GC）B细胞分化和凋亡的细胞和分子因素。在维持GC B细胞存活的培养系统中，在存在IL-2、IL-4和IL-10的情况下，CD40L刺激对于GC B细胞的增殖和分化至关重要。IL-2和IL-4促进GC B细胞的增殖，而IL-10是产生浆细胞所必需的。记忆B细胞的产生需要CD40L、IL-2、IL-4，但不需要IL-10。有两种导致凋亡的机制。在早期，在没有CD40刺激的情况下会发生自发凋亡。在CD40L刺激后，Fas介导的凋亡作用于消除GC B细胞，除非活化的GC B细胞通过B细胞Ig受体遇到第二个信号。讨论了这些发现的生理学意义。
