Role of the major histocompatibility complex in T cell activation of B cell subpopulations. Major histocompatibility complex-restricted and -unrestricted B cell responses are mediated by distinct B cell subpopulations.
Role of the major histocompatibility complex in T cell activation of B cell subpopulations. Major histocompatibility complex-restricted and -unrestricted B cell responses are mediated by distinct B cell subpopulations.
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DOI：
10.1084/jem.154.4.1100
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发表时间：
1981-10-01
期刊：
影响因子：
--
通讯作者：
Hodes RJ
中科院分区：
文献类型：
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作者：
Asano Y;Singer A;Hodes RJ
本研究评价了参与T依赖性抗体应答的B细胞亚群的身份，所述T依赖性抗体应答在其对主要组织相容性复合物限制性T细胞识别的要求方面不同。研究了匙孔血蓝蛋白（KLH）致敏的T细胞和三硝基苯基（TNP）致敏的B细胞对低浓度和高浓度抗原TNP-KLH的体外应答。首次证明，对于低浓度TNP-KLH的应答，（A × B）F（1）{arrow}亲本（A）嵌合辅助T细胞识别亲本（A）而非亲本（B）H-2决定簇的能力受到限制，所述H-2决定簇由B细胞和抗原呈递细胞（APC）表达。相反，在较高的抗原浓度下，辅助性T细胞与B细胞的相互作用不受限制。然后确定这些观察到的T细胞识别差异是否是由具有不同活化要求的不同B细胞亚群的活化引起的。在低浓度的TNP-KLH下，证明了LyB-5（-）B细胞被激活，因此在这些条件下，LyB-5（-）亚群的激活需要T细胞识别B细胞H-2。相反，对高浓度抗原的应答需要LyB-5（+）B细胞的参与，并且这些LyB-5（+）B细胞通过需要H-2限制性T细胞与APC相互作用的途径而被激活，但不与B细胞相互作用。本文所述的结果表明，LyB-5（-）和LyB-5（+）B细胞构成B细胞亚群，其对TNP-KLH的T细胞依赖性抗体应答的活化要求显著不同。这样做，这些发现已经确定，遗传限制在免疫应答调节中的功能严重依赖于功能不同的B淋巴细胞亚群以及T淋巴细胞所采用的活化途径。
The present study has evaluated the identity of the B cell subpopulations participating in T dependent antibody responses that differ in their requirements for major histocompatibility complex-restricted T cell recognition. In vitro responses of keyhole limpet hemocyanin (KLH)-primed T cells and trinitrophenyl (TNP)-primed B cells were studied to both low and high concentrations of the antigen TNP-KLH. It was first demonstrated that for responses to low concentrations of TNP-KLH, (A × B)F(1) {arrow} parent(A) chimeric helper T cells were restricted in their ability to recognize parent(A) but not parent(B) H-2 determinants expressed by both B cells and antigen-presenting cells (APC). In contrast, at higher antigen concentrations, helper T cells were not restricted in their interaction with B cells. It was then determined whether these observed differences in T cell recognition resulted from the activation of distinct B cell subpopulations with different activation requirements. At low concentrations of TNP-KLH it was demonstrated that Lyb-5(-) B cells were activated, and that it was thus the activation of the Lyb-5(-) subpopulation that required T cell recognition of B cell H-2 under these conditions. In contrast, responses to high concentration of antigen required the participation of Lyb-5(+) B cells, and these Lyb-5(+) B cells were activated by a pathway that required H-2- restricted T cell interaction with APC, but not with B cells. The findings presented here have demonstrated that Lyb-5(-) and Lyb-5(+) B cells constitute B cell subpopulations that differ significantly in their activation requirements for T cell-dependent antibody responses to TNP-KLH. In so doing, these findings have established that the function of genetic restrictions in immune response regulation is critically dependent upon the activation pathways employed by functionally distinct subpopulations of B, as well as T, lymphocytes.