自引率: 4.2%
被引量: 1145
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国人发稿量: 5
投稿须知/期刊简介:
The mission of Transplant Immunology is to disseminate information regarding the study of transplantation pathobiology, to serve as a forum for new ideas and concepts in clinical and experimental transplantation, to foster the evolution of the discipline and to assist transplant investigators in their professional endeavours. Transplantation pathobiology encompasses organ preservation, ischaemia/reperfusion injury, hyperacute rejection and xenotransplantation, acute and chronic rejection, and tissue anomalies that develop in association with transplantation. Although immunology plays a significant part in transplant pathobiology, other factors related to organ physiology, acute and chronic inflammation, vascular biology, cell biology, tissue repair/remodelling, cellular signalling and gene expression are important contributors to these pathologic processes. Studies in all of these areas are suitable for publication in Transplant Immunology. Investigators are encouraged to submit the results of in vitro and in vivo studies that fall anywhere along the spectrum from basic research to preclinical and clinical research. Transplant Immunology also seeks reports on therapeutic agents and approaches, including transplant-related gene therapy strategies. Submitted manuscripts will be rapidly peer-reviewed and published. They will be judged on the basis of scientific merit, originality, timeliness and quality. In addition, Transplant Immunology will publish features intended to help evaluate issues, highlight advancements or assist investigators in their professional endeavours. Unsolicited suggestions and contributions for these features are encouraged.
期刊描述简介:
Transplant Immunology will publish up-to-date information on all aspects of the broad field it encompasses. The journal will be directed at (basic) scientists, tissue typers, transplant physicians and surgeons, and research and data on all immunological aspects of organ-, tissue- and (haematopoietic) stem cell transplantation are of potential interest to the readers of Transplant Immunology. Original papers, Review articles and Hypotheses will be considered for publication and submitted manuscripts will be rapidly peer-reviewed and published. They will be judged on the basis of scientific merit, originality, timeliness and quality.
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Peripheral tolerance in transgenic mice expressing class I MHC L(d) only on cardiac cells.
The fate of autoreactive T cells exposed to extrathymic self-antigen is examined in a double transgenic (DTG) mouse [(L(d+) cardiacx2C)F1], where cardiac myocytes alone express L(d) and T cells express an antigen receptor (2C TCR) against L(d). Naïve cardiac L(d+) single transgenic (STG) mice (before breeding with 2C) and DTG mice were examined for evidence of autoimmunity. The L(d+) STG hearts were then transplanted to syngeneic L(d-) wild type C57BL/6 to evaluate the heart's immunogenicity. L(d+) skin grafts were transplanted to non-transgenic B6, transgenic 2C, STG, and DTG mice. Phenotype analysis of peripheral 1B2+(identifies 2C T cells), CD4+, and CD8+ T cells was performed by FACS. In vitro MLC and CTL, with and without the addition of IL-2 and suppressor cell assays, were evaluated. Neither STG nor DTG hearts developed any evidence of autoimmunity by histology. In contrast, B6 mice rejected the L(d+) STG heart in 17+/-9.7 days (P<0.01), while a syngeneic B6 heart transplant was accepted indefinitely. Survival of L(d+) skin grafts was prolonged in both STG and DTG mice. FACS quantitation revealed that while there was no deletion of peripheral 2C cells in the DTG, these 2C T cells did have a significantly reduced proliferative and cytotoxic response to H-2L(d). Restoration of the proliferative and cytotoxic response of the DTG cells by the addition of IL-2 was consistent with a state of anergy. These findings suggest that the expression of extrathymic class I MHC expression alone did not trigger autoimmune reactions but that the T cells can be rendered anergic to the specific 'self' antigen.
被引量：- 发表：2004
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Mechanism of portal venous tolerant long-term MHC Class I L(d)-specific skin graft survival in transgenic 2CF1 mice.
Administration of alloantigen via the portal vein (PV) in non-transgenic animals has been shown to promote immunologic tolerance and enhance transplant allograft survival. The underlying mechanisms remain unclear. In 2C x dm2 F1 (2CF1) transgenic mice, the monoclonal antibody, 1B2, identifies specific 2C TCR transgenic CD8+ T cells that are cytotoxic against Class I MHC L(d). In these mice, the specific response by these cells to L(d+) skin grafts after PV administration of L(d+) antigen was determined. Saline (control) or allogeneic C57BL/6 x BALB/c F1 (CB6F1) spleen cells (25 x 10(6)), which differ from 2CF1 only at L(d), were injected PV into 2CF1 mice. One week later, CB6F1 tail skin was transplanted onto the dorsum of these 2CF1 mice. Skin graft rejection was defined as >50% loss of the graft. Parallel experiments were performed in non-transgenic littermates [B6F1 (C57BL/6 x dm2)]. FACS analysis of 2CF1 peripheral blood for 1B2+, CD4+, and CD8+ T cells was performed 2 days before PV injection (9 days prior to skin grafting), 5 days after PV injection (2 days prior to skin grafting), and 7, 14, 21, 28, and 60 days after skin grafting. FACS analysis of nai;ve, saline control, and CB6F1 PV-treated 2CF1 thymocytes was also performed. Responsiveness of saline (control)-treated and PV-treated 2CF1 splenocytes was measured by in vitro cytotoxic T lymphocyte (CTL). All CB6F1 skin grafts were rejected in <14 days by PV saline controls. However, a single PV injection of donor L(d+) CB6F1 cells was sufficient to induce indefinite CB6F1 (L(d+)) skin allograft survival in 100% of non-transgenic B6F1 and transgenic 2CF1 (anti-L(d)) TCR transgenic recipients. FACS analysis of 1B2+ T cells demonstrated that PV injection of donor antigen followed by a CB6F1 skin graft led to a 70% decrease in peripheral donor-reactive 1B2+ CD8+ T cells by day 7, while central thymocytes were unchanged. CTL of 2CF1 splenocytes following PV CB6F1 demonstrated that they were hyporesponsive to L(d) compared to saline-treated 2CF1 splenocytes. Despite recovery of peripheral CD8+ T cells to near normal levels by 60 days post-transplantation, skin graft survival persisted indefinitely. Administration of specific PV antigen results in exquisite long-term L(d+) skin allograft acceptance. This tolerance induction is related to a significant peripheral deletion of donor-reactive 1B2+ CD8+ transgenic T cells and anergy of the residual T cells.
被引量：- 发表：2003
