| B7(+)-transfectant tubular epithelial cells induce T cell anergy, ignorance or proliferation. | |
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MedLine Citation:
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PMID: 8007580 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We have previously established that interferon (IFN)-gamma stimulated, antigen-pulsed tubular epithelial cells (TEC) stimulate antigen (Ag) specific activation of T cell hybridomas to express IL-2. In contrast, these Ag pulsed TEC do not stimulate T helper 1 (Th1) clones to proliferate, but rather render them unresponsive, since Ag pulsed spleen cells cannot restore these cells to proliferate. The interaction of the T cell CD28 surface protein with its ligand B7 expressed on Ag presenting cells bearing Ia is a potent co-stimulatory signal capable of inducing T cell proliferation. Hence, the lack of B7 on TEC was hypothesized to be responsible for anergy in these Th1 cells. Therefore, the B7 gene was transfected into a SV40 transformed TEC or Chinese hamster ovary (CHO) cells, and created TEC and CHO cells expressing surface B7 protein. TEC-B7 (IFN-gamma stimulated, Ag pulsed) express Ia and induce IL-2 production by T cell hybridomas. In contrast, T cell proliferation was not induced by TEC-B7 or CHO-B7 cells; however, these Th1 cells were not anergic since they could be stimulated to proliferate to Ag pulsed spleen cells (immunological ignorance). However, co-cultivating TEC- B7 (IFN-gamma stimulated, Ag pulsed) with Th1 cells stimulated through the T cell receptor (TCR) using anti-CD3 monoclonal antibody (mAb) caused these Th1 cells to proliferate. Furthermore, anti-CD28 and anti-B7 mAbs blocked this response.(ABSTRACT TRUNCATED AT 250 WORDS) |
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Authors:
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H Yokoyama; X Zheng; T B Strom; V R Kelley |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Kidney international Volume: 45 ISSN: 0085-2538 ISO Abbreviation: Kidney Int. Publication Date: 1994 Apr |
Date Detail:
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Created Date: 1994-07-18 Completed Date: 1994-07-18 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0323470 Medline TA: Kidney Int Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1105-12 Citation Subset: IM |
Affiliation:
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Department of Medicine, Harvard Medical School, Boston, Massachusetts. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antibodies, Monoclonal / immunology Antigen Presentation / immunology Antigen-Presenting Cells / immunology Antigens, CD28 / immunology Cell Line Clonal Anergy / immunology* Epithelium / immunology Female Histocompatibility Antigens Class II / immunology Kidney Tubules, Proximal / immunology* Ligands Lymphocyte Activation / immunology* Mice Mice, Inbred C3H Spleen / immunology T-Lymphocytes / immunology* Transfection* |
| Grant Support | |
ID/Acronym/Agency:
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DK-36149/DK/NIDDK NIH HHS; DK-40839/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antibodies, Monoclonal; 0/Antigens, CD28; 0/Histocompatibility Antigens Class II; 0/Ligands |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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