Rejection Of Allografts In Mice
Mostrando 1-12 de 38 artigos, teses e dissertações.
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1. The imbalance between Treg and Th17 cells caused by FTY720 treatment in skin allograft rejection
OBJECTIVES: FTY720 modulates CD4+T cells by the augmentation of regulatory T cell activity, secretion of suppressive cytokines and suppression of IL-17 secretion by Th17 cells. To further understand the process of graft rejection/acceptance, we evaluated skin allograft survival and associated events after FTY720 treatment. METHODS: F1 mice (C57BL/6xBALB/c) a
Clinics. Publicado em: 2012-07
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2. Participation of B-1 cells in the rejection of allografts. / Participação de células B-1 na rejeição de aloenxertos no camundongo.
B-1 B cells are important producers of natural antibodies in mice and humans and, therefore, are considered as the first line of defense against pathogens. Because of that, their role in T-cell mediated immune responses is commonly underrated. However, recent studies have described the participation of B-1 cells in immediate and delayed-type hypersensitivity
Publicado em: 2009
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3. Da tolerância oral e seus efeitos indiretos na transferência adotiva singênica e na rejeição de aloenxertos
Oral tolerance is characterized by a reduction in specific immunological activities to a protein previously given by oral route. Parenteral exposure to antigens to which oral tolerance had been previously induced affects (inhibits) immunological activities connected to unrelated antigens, a phenomenon we have called indirect effects of oral tolerance. Herein
Publicado em: 2009
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4. The role of CD8+ T cells during allograft rejection
Organ transplantation can be considered as replacement therapy for patients with end-stage organ failure. The percent of one-year allograft survival has increased due, among other factors, to a better understanding of the rejection process and new immunosuppressive drugs. Immunosuppressive therapy used in transplantation prevents activation and proliferation
Brazilian Journal of Medical and Biological Research. Publicado em: 2002-11
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5. Targeting of the chemokine receptor CCR1 suppresses development of acute and chronic cardiac allograft rejection
Although mononuclear cell infiltration is a hallmark of cellular rejection of a vascularized allograft, efforts to inhibit rejection by blocking leukocyte-endothelial cell adhesion have proved largely unsuccessful, perhaps in part because of persistent generation of chemokines within rejecting grafts. We now provide, to our knowledge, the first evidence that
American Society for Clinical Investigation.
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6. Evidence that the effector mechanism of skin allograft rejection is antigen-specific.
In vivo rejection responses are initiated by specific T-cell recognition of foreign histocompatibility antigens expressed by tissue allografts, but it is not certain if the effector mechanism mediating the actual tissue injury is also antigen-specific. To directly assess the specificity of the effector phase of in vivo rejection responses, we constructed B6
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7. Prolongation of murine islet allograft survival by pretreatment of islets with antibody directed to Ia determinants.
Islets of Langerhans treated with donor-specific anti-Ia serum and complement were transplanted across a major histocompatibility barrier into nonimmunosuppressed diabetic mice. The allografts survived in all recipients for at least 200 days after transplantation. Rejection of an established allograft could be induced by intravenous injection of donor spleno
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8. Influence of polyunsaturated fatty acids on survival of skin allografts and tumor incidence in mice.
Subcutaneous or oral administration of the polyunsaturated fatty acid linoleic acid prolongs survival of skin allografts in mice. Mice fed on a diet deficient in polyunsaturated fatty acids show a relative immunopotentiation, as indicated by accelerated skin allograft rejection and decreased incidence and rate of development of methylcholanthrene-induced tum
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9. Demonstration of active tolerance in maintenance of established islet of Langerhans allografts.
Streptozotocin-induced diabetes in mice can be reversed by transplantation of islets of Langerhans from histoincompatible mice if the islets are treated with anti-Ia-serum and complement before transplantation. Here we show that anti-Ia-treated islets most likely induce tolerance in the recipient animals. Daily injections of recipient-specific anti-I-J-serum
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10. Pancreatic islet production of murine interleukin-10 does not inhibit immune-mediated tissue destruction.
IL-10 inhibits macrophage-dependent antigen presentation, cytokine production, and generation of allospecific cells in vitro. These findings have lead to the widespread expectation that IL-10 may be a useful immunosuppressive agent to inhibit allograft rejection or autoimmunity in vivo. We used two experimental paradigms to study effects of murine IL-10 on i
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11. Interferon-gamma deficiency prevents coronary arteriosclerosis but not myocardial rejection in transplanted mouse hearts.
We have hypothesized that T cell cytokines participate in the pathogenesis of graft arterial disease (GAD). This study tested the consequences of IFN-gamma deficiency on arterial and parenchymal pathology in murine cardiac allografts. Hearts from C-H-2(bm12)KhEg (bm12, H-2(bm12)) were transplanted into C57/B6 (B6, H-2(b)), wild-type, or B6 IFN-gamma-deficien
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12. Monokine Induced by Interferon-γ (MIG/CXCL9) Is Derived from Both Donor and Recipient Sources during Rejection of Class II Major Histocompatibility Complex Disparate Skin Allografts
Chemokines, including monokine induced by interferon-γ (Mig/CXCL9), are produced both in allografts and during the direct T-cell infiltration that mediates graft rejection. Neither the specific production nor contribution of allograft donor versus recipient Mig in allograft rejection is currently known. C57BL/6 mice with a targeted deletion in the Mig gene
American Society for Investigative Pathology.