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The potentiation of B lymphocyte responses through CD2/LFA-3 interactions involving erythrocytes is IL2 independent.

作者信息

Trifiletti R, La Via M, Virella G

机构信息

Department of Pathology, Medical University of South Carolina, Charleston 29425.

出版信息

Cell Immunol. 1989 Dec;124(2):359-67. doi: 10.1016/0008-8749(89)90137-8.

DOI:10.1016/0008-8749(89)90137-8
PMID:2479486
Abstract

The response of human B cells to pokeweed mitogen (PWM) stimulation is potentiated when autologous erythrocytes (E) are added to peripheral blood mononuclear cell (PBMC) cultures. This potentiation has been previously shown to be dependent on interactions between the CD2 molecule on T cells and the lymphocyte function-associated antigen 3 (LFA-3) expressed by autologous erythrocytes. Since in other experimental systems the activation of T cells by CD2/LFA-3 interactions has resulted in increased secretion of interleukin 2 (IL2), we were interested in studying the role of IL2 in PBMC cultures stimulated with PWM and autologous E. The addition of autologous E significantly depressed IL2 levels in PWM-stimulated PBMC cultures. This effect was not secondary to increased expression of IL2 receptors by activated cells, since the addition of anti-TAC antibodies did not result in a significant increase in measurable levels of IL2. The addition of anti-IL2 to PBMC failed to abrogate the potentiating effect of E and it actually further enhanced the production of IgM and IgG from cultures stimulated with PWM + E. These results suggest that the potentiation of B cell function induced by autologous E is not mediated by IL2, either directly or indirectly. It is possible that the effect of autologous E either is mediated by other interleukins or is dependent on cell-to-cell contact with directed release of IL2 and/or other lymphokines without detectable secretion to the extracellular compartment.

摘要

相似文献

1
The potentiation of B lymphocyte responses through CD2/LFA-3 interactions involving erythrocytes is IL2 independent.
Cell Immunol. 1989 Dec;124(2):359-67. doi: 10.1016/0008-8749(89)90137-8.
2
The interaction of CD2 with its LFA-3 ligand expressed by autologous erythrocytes results in enhancement of B cell responses.
Cell Immunol. 1988 Oct 15;116(2):308-19. doi: 10.1016/0008-8749(88)90233-x.
3
The stimulation of T cells with anti-CD2 monoclonal antibodies facilitates the induction of polyclonal B-cell responses but does not enhance the activation of antigen-specific B cells.用抗CD2单克隆抗体刺激T细胞有助于诱导多克隆B细胞反应,但不会增强抗原特异性B细胞的活化。
Scand J Immunol. 1990 Jan;31(1):25-31. doi: 10.1111/j.1365-3083.1990.tb02739.x.
4
Enhancement of B cell responses by the interaction of CD2 with LFA-3.
J Tongji Med Univ. 1992;12(2):71-4. doi: 10.1007/BF02887783.
5
Requirement for both the CD3/T cell receptor complex and the CD2/lymphocyte function-associated antigen-3 adhesion system in monocyte-independent T cell activation by oxidized erythrocytes.氧化红细胞在不依赖单核细胞的T细胞活化中对CD3/T细胞受体复合物和CD2/淋巴细胞功能相关抗原-3黏附系统的需求。
Immunol Invest. 1989 Nov-Dec;18(9-10):1081-93. doi: 10.3109/08820138909030609.
6
Synergistic T cell activation via the physiological ligands for CD2 and the T cell receptor.通过CD2的生理配体和T细胞受体实现协同性T细胞激活。
J Exp Med. 1988 Sep 1;168(3):1145-56. doi: 10.1084/jem.168.3.1145.
7
Remote T cell co-stimulation via LFA-1/ICAM-1 and CD2/LFA-3: demonstration with immobilized ligand/mAb and implication in monocyte-mediated co-stimulation.通过LFA-1/ICAM-1和CD2/LFA-3进行的远程T细胞共刺激:固定化配体/单克隆抗体的验证及其在单核细胞介导的共刺激中的意义
Eur J Immunol. 1991 Jul;21(7):1711-8. doi: 10.1002/eji.1830210719.
8
Inhibition by anti-CD2 monoclonal antibodies of anti-CD3-induced T cell-dependent B cell activation.
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9
Specific interaction of lymphocyte function-associated antigen 3 with CD2 can inhibit T cell responses.淋巴细胞功能相关抗原3与CD2的特异性相互作用可抑制T细胞反应。
J Exp Med. 1993 Jul 1;178(1):211-22. doi: 10.1084/jem.178.1.211.
10
Functional CD2 mutants unable to bind to, or be stimulated by, LFA-3.无法与淋巴细胞功能相关抗原-3(LFA-3)结合或被其刺激的功能性CD2突变体。
J Immunol. 1990 Feb 15;144(4):1215-20.

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