CD40 and B cell antigen receptor dual triggering of resting B lymphocytes turns on a partial germinal center phenotype.

CD40 and B cell antigen receptor dual triggering of resting B lymphocytes turns on a partial germinal center phenotype.
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DOI:
10.1084/jem.183.1.77
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发表时间:
1996-01-01
影响因子:
15.3
通讯作者:
Rousset, F
Rousset, F
中科院分区:
医学1区
文献类型:
--
作者:
Galibert, L;Burdin, N;deSaintVis, B;Garrone, P;VanKooten, C;Banchereau, J;Rousset, F

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当静息的人 B 淋巴细胞变成生发中心 (GC) 细胞时,就会发生表型改变。这些包括表面 CD38、CD95 (FAS/APO-1) 和羧肽酶-M (CPM)(最近描述的 GC 标记)的诱导。然而,控制这些表面分子在 B 细胞上的体内诱导的因素仍然未知。在这里,我们从扁桃体中纯化了静息 (CD38-) 人 B 淋巴细胞,试图建立诱导这三种 GC 标记物的培养条件。我们发现干扰素 (IFN) α 或 IFN-γ 以及抗 B 细胞抗原受体 (BCR) 的抗体可以诱导静息 B 淋巴细胞上的 CD38,这种现象通过 CD40 刺激进一步增强。与此同时,CD95 通过 CD40 连接上调,并在较小程度上通过 IFN-γ 上调。相比之下,CPM 表达只能通过 BCR 触发来上调。 CD19 或 CD40 连接特别增强了这种 CPM 诱导。在交联抗 BCR 单克隆抗体存在下,用 CD40 配体转染的成纤维细胞对静息 B 细胞进行 CD40 + BCR 刺激,导致 CD38、CD95 和 CPM 的共表达。作为 GC 细胞,这些细胞还表达 CD71、CD80 (B7.1) 和 CD86 (B7.2),但不表达 CD24。然而,在这些培养条件下无法检测到 CD10+ 或 CD44- B 细胞,这表明诱导这些 GC 标记还需要其他信号。与 GC 表型一致,CD40 + BCR 刺激的细胞在没有刺激的情况下培养 20 小时时表现出活力降低。这些结果首先证明,通过 BCR 和 CD40 共同触发静息 B 细胞可诱导表型和功能性 GC 特征。他们还表明,静息 B 细胞的 IFN 和 CD19 触发特异性调节 GC 标记物的表达。
Phenotypic alterations occur when resting human B lymphocytes become germinal center (GC) cells. These include the induction of surface CD38, CD95 (FAS/APO-1), and carboxy-peptidase-M (CPM), a recently described GC marker. However, the factors that govern the in vivo induction of these surface molecules on B cells remain unknown. Here, we purified resting (CD38-) human B lymphocytes from tonsils in an attempt to establish culture conditions resulting in the induction of these three GC markers. We show that interferon (IFN) alpha or IFN- gamma, as well as antibodies against the B cell antigen receptor (BCR), could induce CD38 on resting B lymphocytes, a phenomenon further enhanced by CD40 stimulation. Concomitantly, CD95 was upregulated by CD40 ligation and, to a lesser extent, by IFN-gamma. By contrast, CPM expression could be upregulated only through BCR triggering. This CPM induction was specifically enhanced by CD19 or CD40 ligation. CD40 + BCR stimulation of resting B cells with CD40 ligand-transfected fibroblastic cells in the presence of cross-linked anti-BCR monoclonal antibodies resulted in the coexpression of CD38, CD95, and CPM. As GC cells, these cells also expressed CD71, CD80 (B7.1), and CD86 (B7.2), but not CD24. However, CD10+ or CD44- B cells could not be detected in these culture conditions, suggesting that yet other signals are required for the induction of these GC markers. Consistent with a GC phenotype, CD40 + BCR-stimulated cells exhibited reduced viability when cultured for 20 h in the absence of stimulus. These results first demonstrate that cotriggering of resting B cells through BCR and CD40 induces both phenotypic and functional GC features. They also show that IFN and CD19 triggering of resting B cells specifically modulate the expression of GC markers.
DOI: 10.1084/jem.179.2.425
发表时间: 1994-02-01
期刊: The Journal of experimental medicine
影响因子: --
作者:
Cooke MP;Heath AW;Shokat KM;Zeng Y;Finkelman FD;Linsley PS;Howard M;Goodnow CC
通讯作者: Goodnow CC
FAS结扎诱导CD40激活的人B淋巴细胞的凋亡。
DOI: 10.1084/jem.182.5.1265
发表时间: 1995-11-01
影响因子: 15.3
作者:
Garrone, Pierre;Neidhart, Eve-Marie;Garcia, Eric;Galibert, Laurent;Van Kooten, Cees;Banchereau, Jacques
通讯作者: Banchereau, Jacques
DOI: 10.1084/jem.180.1.191
发表时间: 1994-07-01
期刊: The Journal of experimental medicine
影响因子: --
作者:
Maloney MD;Lingwood CA
通讯作者: Lingwood CA
DOI: 10.1016/0092-8674(93)90668-g
发表时间: 1993-01-29
期刊: CELL
影响因子: 64.5
作者:
ARUFFO, A;FARRINGTON, M;OCHS, HD
通讯作者: OCHS, HD
DOI: 10.1038/361539a0
发表时间: 1993-02-11
期刊: NATURE
影响因子: 64.8
作者:
KORTHAUER, U;GRAF, D;KROCZEK, RA
通讯作者: KROCZEK, RA