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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Ishii, Daisuke Baldwin, William M. Nozaki, Taiji Rosenblum, Joshua M. Setoguchi, Kiyoshi Schenk, Austin D. Su, Charles A. Gorbacheva, Victoria Valujskikh, Anna Fairchild, Robert L. |
| Description | Author Affiliation: Ishii D ( Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195); Rosenblum JM ( Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195); Nozaki T ( Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195); Schenk AD ( Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195); Setoguchi K ( Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195); Su CA ( Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195); Gorbacheva V ( Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195); Baldwin WM ( Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195); Valujskikh A ( Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195); Fairchild RL ( Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195) |
| Abstract | Recipient CD4 T regulatory cells inhibit the acute T cell-mediated rejection of renal allografts in wild-type mice. The survival of single class II MHC-disparate H-2(bm12) renal allografts was tested in B6.CCR5(-/-) recipients, which have defects in T regulatory cell activities that constrain alloimmune responses. In contrast to wild-type C57BL/6 recipients, B6.CCR5(-/-) recipients rejected the bm12 renal allografts. However, donor-reactive CD8 T cells rather than CD4 T cells were the primary effector T cells mediating rejection. The CD8 T cells induced to bm12 allografts in CCR5-deficient recipients were reactive to peptides spanning the 3 aa difference in the I-A(bm12) versus I-A(b) ß-chains presented by K(b) and D(b) class I MHC molecules. Allograft-primed CD8 T cells from CCR5-deficient allograft recipients were activated during culture either with proinflammatory cytokine-stimulated wild-type endothelial cells pulsed with the I-A(bm12) peptides or with proinflammatory cytokine-simulated bm12 endothelial cells, indicating their presentation of the I-A(bm12) ß-chain peptide/class I MHC complexes. In addition to induction by bm12 renal allografts, the I-A(bm12) ß-chain-reactive CD8 T cells were induced in CCR5-deficient, but not wild-type C57BL/6, mice by immunization with the peptides. These results reveal novel alloreactive CD8 T cell specificities in CCR5-deficient recipients of single class II MHC renal allografts that mediate rejection of the allografts. |
| ISSN | 00221767 |
| e-ISSN | 15506606 |
| DOI | 10.4049/jimmunol.1303256 |
| Journal | The Journal of Immunology |
| Issue Number | 7 |
| Volume Number | 193 |
| Language | English |
| Publisher | The American Association of Immunologists |
| Publisher Date | 2014-10-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cd8-positive T-lymphocytes Immunology Graft Rejection Histocompatibility Antigens Class Ii Kidney Transplantation Receptors, Ccr5 Allografts Animals Pathology Cytokines Genetics H-2 Antigens Mice Mice, Knockout Research Support, N.i.h., Extramural Discipline Immunology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Immunology and Allergy Immunology |
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