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克隆型的改变。二、关于BALB/c脾B细胞维持对磷酸胆碱的反应性及T15独特型优势能力的研究。

Alteration of clonal profile. II. Studies on the capacity of BALB/c splenic B cells to perpetuate responsiveness to phosphorylcholine and T 15 idiotypic dominance.

作者信息

Quintáns J, Loken M R, Quan Z S, Dick R F, Regueiro B

出版信息

Eur J Immunol. 1981 Mar;11(3):236-41. doi: 10.1002/eji.1830110313.

Abstract

(CBA/N x BALB/c)F1 hybrid male mice are unable to mount anti-phosphorylcholine (PC) plaque-forming cell (PFC) responses because they carry the CBA/N X-linked immune defect of B lymphocyte differentiation. Transplantation of splenic B cells from BALB/c mice restores responsiveness to thymus-dependent and thymus-independent PC antigens up to 8 months after cell transfer. Cytotoxicity studies demonstrate the donor origin of PFC generated in reconstituted (CBA/N x BALB/c)F1 mice. Although responsiveness to PC is restored permanently, a shift in idiotype expression that leads to the loss of T 15 idiotypic dominance 3 months after cell transfer can be detected. This shift originates from Ig- cells because Ig+ splenic cells purified in a fluorescence-activated cell sorter maintain T 15 dominance. Therefore, the Ig+ cells have a remarkable capacity to maintain responsiveness to antigens and can perpetuate idiotypic dominance if the stem cell pool is removed.

摘要

(CBA/N×BALB/c)F1 杂交雄性小鼠无法产生抗磷酸胆碱(PC)的空斑形成细胞(PFC)反应,因为它们携带 B 淋巴细胞分化的 CBA/N X 连锁免疫缺陷。从 BALB/c 小鼠移植脾 B 细胞可恢复对胸腺依赖性和胸腺非依赖性 PC 抗原的反应性,直至细胞转移后 8 个月。细胞毒性研究证明了在重建的(CBA/N×BALB/c)F1 小鼠中产生的 PFC 的供体来源。尽管对 PC 的反应性永久恢复,但在细胞转移 3 个月后可检测到独特型表达的转变,导致 T15 独特型优势丧失。这种转变源于 Ig-细胞,因为在荧光激活细胞分选仪中纯化的 Ig+脾细胞维持 T15 优势。因此,如果去除干细胞池,Ig+细胞具有维持对抗原反应性的显著能力,并且可以使独特型优势永久存在。

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