Beta 2-adrenoceptor stimulation increases the number of antigen-specific precursor B lymphocytes that differentiate into IgM-secreting cells without affecting burst size.
Beta 2-adrenoceptor stimulation increases the number of antigen-specific precursor B lymphocytes that differentiate into IgM-secreting cells without affecting burst size.
复制标题
Beta 2-肾上腺素受体刺激会增加抗原特异性前体 B 淋巴细胞的数量，这些淋巴细胞可分化为 IgM 分泌细胞，而不影响爆发大小。
作者：
V. Sanders;F. E. Powell
以前的研究表明，在SRBC免疫的全脾细胞培养中早期加入β2-肾上腺素能激动剂，可以诱导分泌抗原特异性抗体的细胞数量增加。由于这些培养物中抗原特异性B淋巴细胞的频率很低，因此很难确定产生这种增加的细胞机制。为了深入了解这一细胞机制，本研究旨在评估在高密度和有限稀释条件下培养的TNP特异性B淋巴细胞与锁孔血蓝蛋白(KLH)特异性、产生IL-4的Th淋巴细胞和β2肾上腺素能激动剂特布他林的反应性。结果表明，特布他林暴露的淋巴细胞经5天批量培养后，抗TNP IgM分泌细胞数和抗TNP IgM分泌量均最大增加一倍。这种反应以浓度依赖的方式发生，并被β-肾上腺素能受体拮抗剂伴随培养所抑制。特布他林+银暴露的原代培养细胞的IgG1分泌水平和特布他林+银暴露的TNP特异性B淋巴细胞的MHC-II类表达水平与单独的银暴露相比没有明显变化。这些数据提出了这样一种可能性，即刺激β2-肾上腺素能受体诱导更大比例的TNP特异性B淋巴细胞前体细胞分化为抗TNP IgM分泌细胞，或者诱导恒定数量的TNP特异性B淋巴细胞前体细胞的广泛增殖，或者两者兼而有之。极限稀释结果显示，刺激β2肾上腺素能受体诱导分化为抗TNP IgM分泌细胞的TNP特异性B淋巴细胞前体细胞数量增加一倍，但不影响每个前体克隆产生的抗TNP IgM分泌细胞的数量。
Previous studies have shown that early addition of a beta 2-adrenergic agonist to whole splenocyte cultures immunized with SRBC induced an increase in the number of cells secreting Ag-specific antibody. Because of the low frequency of Ag-specific B lymphocytes in these cultures, it has been difficult to determine the cellular mechanism by which this increase is produced. To gain insight into this cellular mechanism, the present study was designed to evaluate the responsiveness of TNP-specific B lymphocytes cultured at both high density and limiting dilution with keyhole limpet hemocyanin (KLH)-specific, IL-4-producing Th lymphocytes, TNP-KLH, and the beta 2-adrenergic agonist, terbutaline. The results showed that a maximal twofold increase in both the number of anti-TNP IgM-secreting cells and the amount of anti-TNP IgM secretion occurred in terbutaline-exposed lymphocytes after 5 days of bulk culture. This response occurred in a concentration-dependent manner and was inhibited by concomitant culture with beta-adrenoceptor antagonists. No appreciable change was measured in the level of either IgG1 secretion in terbutaline plus Ag-exposed bulk cultures or MHC class II expression on terbutaline plus Ag-exposed TNP-specific B lymphocytes as compared with Ag alone. These data raised the possibility that beta 2-adrenoceptor stimulation induced either the differentiation of a larger proportion of TNP-specific B lymphocyte precursors into anti-TNP IgM-secreting cells, or the extensive proliferation of a constant number of TNP-specific B lymphocyte precursors, or both. Limiting dilution results showed that beta 2-adrenoceptor stimulation induced a twofold increase in the number of TNP-specific B lymphocyte precursors that differentiated into anti-TNP IgM-secreting cells, without affecting the number of anti-TNP IgM-secreting cells produced by each precursor clone.