2 edition of Renal Ia expression in normal mouse and during graft-versus-host disease. found in the catalog.
Renal Ia expression in normal mouse and during graft-versus-host disease.
JosГ© Arturo Wadgymar-Rivera
Written in English
|The Physical Object|
|Number of Pages||49|
Since expression of Ia on TEC induces anergy, this may serve can express Ia during allograft rejection, autoimmune renal injury and graft versus host disease [27—29, 31, 32]. Allogeneic hematopoietic cell or bone marrow transplantation (BMT) causes graft-versus-host-disease (GVHD). However, the involvement of the kidney in acute GVHD is not well-understood. Acute GVHD was induced in Lewis rats (RT1l) by transplantation of Dark Agouti (DA) rat (RT1a) bone marrow cells (× cells) without immunosuppression after lethal irradiation (10 Gy).
M Fujiwara's 24 research works with citations and reads, including: Exocrinopathy resembling Sjogren’s syndrome induced by a murine retrovirus. Thrombotic microangiopathy (TMA) is a major complication after hematopoietic stem cell transplantation (HSCT). In this study, we examined the clinical and pathologic features of 2 patients and 5 autopsy cases with HSCT‐associated renal TMA to clarify the association between graft‐versus‐host disease (GVHD) and renal TMA.
Acute and chronic kidney disease encompasses a complex set of diseases that can both lead to, and result from, cancer. In particular, kidney disease can arise from the use of chemotherapeutic agents. Many of the current and newly developed cancer chemotherapeutic agents are nephrotoxic and can promote kidney dysfunction, which frequently manifests during the terminal stages of cancer. The limiting factor for successful hematopoietic stem cell transplantation (HSCT) is graft-versus-host disease (GvHD), a post-transplant disorder that results from immune-mediated attack of recipient tissue by donor T cells contained in the transplant. Mouse models of GvHD have provided important insights into the pathophysiology of this disease, which have helped to improve the success rate.
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In patients with HCT, multiple factors have been linked to the development of renal impairments, including preexisting renal injury, direct effects of conditioning chemotherapy and irradiation, complications of the infused cryopreserved cells, tumor lysis syndrome, calcineurin inhibitor used for graft-versus-host disease (GVHD) prophylaxis, and Cited by: Demonstration and characterization of Ia-positive dendritic cells in the interstitial connective tissues of rat heart and other tissues, but not brain.
J Exp Med. Aug 1; (2)– [PMC free article] Wadgymar A, Urmson J, Baumal R, Halloran PF. Changes in Ia expression in mouse kidney during acute graft-vs-host disease. J by: Lampert IA, Suitters AJ, Chisholm PM. Expression of Ia antigen on epidermal keratinocytes in graft-versus-host disease.
Nature. Sep 10; ()– Wadgymar A, Urmson J, Baumal R, Halloran PF. Changes in Ia expression in mouse kidney during acute graft-vs-host disease. J Immunol. Apr; (4)–Cited by: 6. Das H, Imoto S, Murayama T, et al. Levels of soluble FasL and FasL gene expression during the development of graft-versus-host disease in DLT-treated patients.
Br J Haematol. ; – Acute renal failure is a common problem after allogeneic hematopoietic stem cell transplantation (allo-SCT) and many factors contribute to its development.
1 Graft-versus-host disease Cited by: 6. Graft-versus-host disease of the kidney after rapid tapering of cyclosporin following reduced intensity hematopoietic stem cell transplantation.
Bone Marrow Transplant ; Cited by: Journal Article: Cyclosporine blocks the induction of class I and class II MHC products in mouse kidney by graft-vs-host disease. Cyclosporine blocks the induction of class I and class II MHC products in mouse kidney by graft-vs-host disease.
Full Record; Other Related Research. A murine model of chronic graft-versus-host disease (GVHD) was induced across minor histocompatibility barriers. This was done by injecting BD2 (H-2d) spleen cells into irradiated BALB/c (H-2d) mice. Chronic GVHD in this model includes features common to human idiopathic scleroderma, such as dermal fibrosis, loss of dermal fat and appendages, and a mononuclear cell filtrate.
To study the effect of immunologic stimuli on renal expression of Ia antigens (the class II products of the major histocompatibility complex), we induced acute graft-vs-host disease (GVHD) in mice and assessed Ia expression in the host kidney. Serologic absorption analyses showed that the amount of host Ia antigen increased up to tenfold in kidney, and immunofluorescence demonstrated that this.
Fine-needle aspiration biopsy specimens of renal transplants were analysed by means of commercially available monoclonal antibodies and an immunoperox. Renal tubulitis and peritubular capillaritis were also noted with a multilayered basement membrane and patchy C4d deposition on peritubular capillaries.
These findings resemble those of chronic antibody‐mediated rejection after kidney transplantation. Furthermore, C4d deposition suggests complement activation. In renal transplantation, incompatibility for class II antigens increases the risk of graft loss from rejection.
In normal kidney, DR antigens are readily demonstrated on vascular endothelium, dendritic cells, and mesangial cells but early studies did not reveal DR on renal tubular cells.I-4 Some DR antigens have been shown in association.
J Urmson's 47 research works with 1, citations and reads, including: Effects of Donor Age and Cell Senescence on Kidney Allograft Survival. Nude mice were injected with normal mouse serum (NMS) to induce keratinocyte expression of the Ia antigen.
The injected mice were then divided into four groups: one was treated with oral CyA; the second was treated topically with CyA twice a day; the third was treated topically with olive oil; and the fourth was injected with nude mouse serum. A murine model of chronic graft-versus-host disease (GVHD) was induced across minor histocompatibility barriers.
This was done by injecting BD2 (H-2 d) spleen cells into irradiated BALB/c (H-2 d) c GVHD in this model includes features common to human idiopathic scleroderma, such as dermal fibrosis, loss of dermal fat and appendages, and a mononuclear cell filtrate. Flowers ME, Inamoto Y, Carpenter PA, Lee SJ, Kiem HP, Petersdorf EW, et al.
Comparative analysis of risk factors for acute graft-versus-host disease and for chronic graft-versus-host disease according to National Institutes of Health consensus criteria. Blood. ; – [PMC free article]. Request PDF | A Systems Immunology Approach to Graft-Versus-Host Disease | Until recently, understanding of immune system organization and function was based on experiments and observations.
Class II (Ia) antigens, in the rat encoded for in the RTlB subregion of the MHC, are potent stimulators of a Graft versus Host Reaction (GvHR) (1). However, the distribution pattern and quantity of Ia antigens expressed on host tissues during a GvHR have not yet been fully established.
Prevention of lethal acute graft-versus-host disease in mice by oral administration of T helper 1 inhibitor, TAK after which weight began to rise, reaching normal levels by day 45 IL p40 messenger RNA expression in target organs during acute graft-versus-host disease: possible involvement of IFN-gamma.
J Immunol. A key feature of Ia expression by many epithelia is its inducibility, for example during graft rejection or a graft-versus-host reaction (Barclay and Mason, ; Suitters and Lampert, ; Benson et al., ), with convincing evidence that the lymphokine interferon is responsible (Pober et al., ).
To study the effect of immunologic stimuli on renal expression of Ia antigens (the class II products of the major histocompatibility complex), we induced acute graft-vs-host disease (GVHD) in mice.().
Changes in Ia expression in the kidney during acute graft-versus-host disease.J. (). Effect of cloned interferon-~" on expression of H-2 and Ia antigens on cell lines of hemopoetic, lymphoid, epithelial, fibroblastic and neuronal origin.
().Graft-versus-host disease (GVHD) is a rare complication after kidney transplantation. We describe a year-old female with end-stage renal disease due to hypertension.