IL-2 dependence of the promotion of human B cell differentiation by IL-6 (BSF-2).
IL-2 dependence of the promotion of human B cell differentiation by IL-6 (BSF-2).
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DOI：
10.4049/jimmunol.144.2.562
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发表时间：
1990-01
影响因子：
4.4
通讯作者：
J. Splawski;Laurie M. Mcanally;P. E. Lipsky
中科院分区：
文献类型：
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作者：
J. Splawski;Laurie M. Mcanally;P. E. Lipsky
本实验观察了rIL-6对高纯度人外周血B细胞生长和分化的影响。IL-6单独诱导未刺激或金黄色葡萄球菌（SA）刺激的B细胞的[3 H]胸苷掺入量最小，并且不增加SA和IL-2诱导的增殖。类似地，单独的IL-6不支持Ig分泌细胞（ISC）的产生或诱导未刺激或SA刺激的B细胞分泌IG。然而，IL-6确实增加了由SA和IL-2诱导的ISC的产生和所有同种型IG的分泌。IL-6对B细胞反应性的最大增强需要其从培养开始时就存在。将IL-6添加到用SA和IL-2刺激的B细胞中延迟超过24小时，降低了其对ISC生成的影响。然而，增加IG生产，但不是ISC的产生时，观察到IL-6加入到B细胞已被SA和IL-2预活化48小时。当活化的B细胞也用IL-2刺激时，这种效应最显著。IL-6与其他细胞因子如IL-1和IL-4的组合在不存在IL-2的情况下不诱导IG的分泌或ISC的产生。此外，IL-6抗体不抑制IL-2对SA刺激的B细胞生长和分化的作用，但抑制IL-6诱导的SA和IL-2刺激的B细胞分泌IG的增加。IL-6单独增强PWM刺激的B细胞分化的T细胞依赖性诱导。这种增强的一部分与其在这些培养物中增加IL-2产生的能力有关。这些结果表明IL-6对B细胞的分化具有几种直接的增强作用，所有这些作用至少部分依赖于IL-2的存在。此外，IL-6可通过增加T细胞产生IL-2而间接增加B细胞分化。
The effect of rIL-6 on the growth and differentiation of highly purified human peripheral blood B cells was examined. IL-6 alone induced minimal incorporation of [3H]thymidine by unstimulated or Staphylococcus aureus (SA)-stimulated B cells and did not augment proliferation induced by SA and IL-2. Similarly, IL-6 alone did not support the generation of Ig-secreting cells (ISC) or induce the secretion of Ig by unstimulated or SA-stimulated B cells. However, IL-6 did augment the generation of ISC and the secretion of all isotypes of Ig induced by SA and IL-2. Maximal enhancement of B cell responsiveness by IL-6 required its presence from the initiation of culture. Delaying the addition of IL-6 to B cells stimulated with SA and IL-2 beyond 24 h diminished its effect on ISC generation. However, increased Ig production but not ISC generation was observed when IL-6 was added to B cells that had been preactivated for 48 h with SA and IL-2. This effect was most marked when the activated B cells were also stimulated with IL-2. IL-6 in combination with other cytokines such as IL-1 and IL-4 did not induce the secretion of Ig or generation of ISC in the absence of IL-2. Moreover, antibody to IL-6 did not inhibit the effect of IL-2 on the growth and differentiation of B cells stimulated with SA, but did inhibit the IL-6-induced augmentation of Ig secretion by B cells stimulated with SA and IL-2. IL-6 alone enhanced T cell dependent induction of B cell differentiation stimulated by PWM. Part of this enhancement was related to its capacity to increase the production of IL-2 in these cultures. These results indicate that IL-6 has several direct enhancing effects on the differentiation of B cells, all of which are at least in part dependent on the presence of IL-2. In addition, IL-6 can indirectly increase B cell differentiation by increasing IL-2 production by T cells.