Effects of Anti-Interleukin-2 Receptor Antibody and Cyclosporin A on Human T Cell Proliferation in Primary Mixed Lymphocyte Reaction

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Title ( eng )
Effects of Anti-Interleukin-2 Receptor Antibody and Cyclosporin A on Human T Cell Proliferation in Primary Mixed Lymphocyte Reaction
Creator
Oiwa Kanae
Sakagami Kenichi
Orita Kunzo
Source Title
Hiroshima Journal of Medical Sciences
Volume 38
Issue 1
Start Page 1
End Page 6
Journal Identifire
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
Abstract
Effects of anti-IL2 receptor antibody (anti-IL2 RAb) and cyclosporin A (CsA) on human T cell proliferation in primary mixed lymphocyte reaction (MLR) were investigated. Both agents inhibited the proliferative response induced by alloantigen in a dose dependent manner when they were added at the initiation of culture. We also analyzed the expression of activation antigen on responder cells and the kinetics of T lymphocyte subset proliferation during MLR using two-color flow cytometry, Cells expressing activation antigens, such as IL-2 receptor and HLA-DR, were found less frequently in anti-IL2 RAb-treated MLR culture (4.8%) than in CsA-treated MLR culture (16.5%) on day 6. Furthermore, proliferation of CD8+CD11- cells, considered a cytotoxic T cell subset, were inhibited significantly more in anti-IL2 RAb-treated MLR culture than in CsA-treated MLR culture. We further demonstrate that CsA inhibits preferentially IL-2 production and anti-IL2 RAb inhibits T cell proliferation by blocking an absorption of IL-2 by activated lymphocytes. These data suggest that anti-IL2 RAb selectively inhibits alloantigen-activated T cells and may prove to be of significant value as an immunosuppressive agent in clinical organ transplantation.
Keywords
Anti-IL2 receptor antibody
Cyclosporin A
Mixed lymphocyte reaction
Two-color flow cytometry
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type departmental bulletin paper
Publisher
Hiroshima University Medical Press
Date of Issued 1989-03
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0018-2052
[NCID] AA00664312
[PMID] 2526799