Renal Ia expression in normal mouse and during graft-versus-host disease. by JosГ© Arturo Wadgymar-Rivera

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In patients with Renal Ia expression in normal mouse and during graft-versus-host disease. book, 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. Consistent with the fibrotic skin disease seen in the BLT GVHD mice and the above expression of IL13, expression of the IL13 target gene, murine Sprr2a, was increased (Figure 3C).

Additionally, we have previously observed that expression of IL13Ra1 correlated with an IL13 response signature in both a mouse model of sclerodermatous GVHD and in.

Expression of Ia-like antigens in normal human non-lymphoid tissues. Graft-versus-host disease induces expression of Ia antigen in rat epidermal cells and gut epithelium. HLA-DR-Iike antigens in the epithelium of the human small intestine. Hormonal regulation of the expression of Ia antigens on mammary gland.

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. Weisdorf D, Haake R, Blazar B, et al. Treatment of moderate/severe acute graft-versus-host disease after allogeneic bone marrow transplantation: an analysis of clinical risk features and outcome.

Blood ; Martin PJ, Schoch G, Fisher L, et al. A retrospective analysis of therapy for acute graft-versus-host disease: secondary treatment. Development of renin expression in the mouse kidney A Sauter1,2, K Machura1,2, B Neubauer1, A Kurtz1 and C Wagner1 1Institut fu ¨r Physiologie der Universitat Regensburg, Regensburg, Germany During metanephric kidney development, renin is expressed in the walls of larger intrarenal arteries, but is.

Loss of antigen-specific CD8+ T cell responses in chronic ethanol mice is accompanied by CD8+ T cell apoptosis and alterations of BIM expression.

(Vols. 34). (6), pp. Alcohol Clin Exp Res. Scroggins, S., Kruckenberg, M. & Schlueter, A. Generation of human regulatory dendritic cells for graft-versus-host disease treatment. Journal Article: Origin of the rat mesangial phagocyte and its expression of the leukocyte common antigen.

Journal Article: Growth regulation of transformed T cells by nonactivated macrophages: the role of Ia expression. Histocompatibility Antigens Class II Subject Areas on Research. Generation of a Mouse Model of Von Hippel-Lindau Kidney Disease Leading to Renal Cancers by Expression of a Constitutively Active Mutant of HIF1α Leiping Fu, 1, 4 Gang Wang, 1, 4 Maria M.

Shevchuk, 2, 4 David M. Nanus, 3, 4 and Lorraine J. Gudas 1, 4, *. Translating Treg cell therapy to the clinic began in the late s with 7 phase 1 clinical trials in graft-versus-host disease, type 1 diabetes, and liver transplantation published by mid In this chapter, we summarize preclinical developments, translational efforts, and clinical implementation of Treg cell therapy in transplantation.

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)–. Graft-versus-host disease (GvHD) is a syndrome, characterized by inflammation in different organs, with the specificity of epithelial cell apoptosis and crypt drop out.

GvHD is commonly associated with stem cell transplants such as those that occur with bone marrow transplants. GvHD also applies to other forms of transplanted tissues such as solid organ transplants.Induction of Lupus in Normal Mouse Strains: Chronic Graft-Versus-Host Disease and Pristane Injection Models, Chronic Graft-Versus-Host Disease, Genetic Alteration of the Expression of Single Molecules, Deletions and Increased Expression, Deleted Molecules in Knockout Mice, Graft-versus-host disease is well recognized in bone marrow transplantation, but has only recently been described in solid organ transplantation.

Two such cases in liver graft recipients, proven by the demonstration of donor type HLA antigens in the peripheral blood and marrow on tissue typing, are described in this paper. The literature on this subject is reviewed and the treatment discussed.

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