Effects of Anti-Interleukin-2 Receptor Antibody and Cyclosporin A on Human T Cell Proliferation in Primary Mixed Lymphocyte Reaction
Hiroshima Journal of Medical Sciences Volume 38 Issue 1
Page 1-6
published_at 1989-03
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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
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Creator |
Oiwa Kanae
Sakagami Kenichi
Orita Kunzo
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Source Title |
Hiroshima Journal of Medical Sciences
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Volume | 38 |
Issue | 1 |
Start Page | 1 |
End Page | 6 |
Journal Identifire |
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
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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.
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Keywords |
Anti-IL2 receptor antibody
Cyclosporin A
Mixed lymphocyte reaction
Two-color flow cytometry
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NDC |
Medical sciences [ 490 ]
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Language |
eng
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Resource Type | departmental bulletin paper |
Publisher |
Hiroshima University Medical Press
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Date of Issued | 1989-03 |
Publish Type | Version of Record |
Access Rights | open access |
Source Identifier |
[ISSN] 0018-2052
[NCID] AA00664312
[PMID] 2526799
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