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Results for “RADIATION IMMUNOLOGY”

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At least 37 records · Page 2Linked to original sources
PubMed1986

A T cell model for age-related loss of homeostasis: identification of the cell type responsible for age-related delay in recovery of the PHA-induced mitogenic response from radiation injury.

Immunologic recovery from radiation injury was used to assess age-related loss of immunologic homeostasis. Mice were exposed to 500 rad to determine whether macrophages, T helper cells and/or T responder cells were responsible for the age-related delay in recovery of PHA-induced mitogenesis. Recovery of macrophages was determined by facilitation of macrophage-deficient cultures, recovery of T helper cells by interleukin 2 production, and recovery of T responder cells by incorporation of tritiated thymidine. The results showed that in old mice macrophages are resistant to radiation and aging, T helper cells recover completely from radiation, and recovery is incomplete for T responder cells.

Aging↗
PubMed2000

Mitogen-activated protein kinase, ERK1/2, is essential for the induction of vascular endothelial growth factor by ionizing radiation mediated by activator protein-1 in human glioblastoma cells.

Vascular Endothelial Growth Factor (VEGF)/Vascular Permeability Factor plays an important role in angiogenesis and cell proliferation of cancer cells. Glioblastoma cells are most malignant and show resistance to radiation therapy inducing VEGF to cause angiogenesis and brain edema. In the present study, the regulatory mechanism of the expression of VEGF by ionizing radiation was studied in three human glioblastoma cells. Induction of VEGF mRNA by ionizing radiation was dependent on dose and incubation time. Activator protein-1 (AP-1) was activated by 10 Gy of ionizing radiation in 1 h in T98G glioblastoma cells on an electrophoretic mobility shift assay. We constructed chimeric genes containing various regions of the VEGF promoter gene and the coding region for chloramphenicol acetyltransferase (CAT) and transiently transfected them to T98G cells. CAT assay with the VEGF promoter gene containing an AP-1 site demonstrated that the promoter activity of the VEGF gene was enhanced by ionizing radiation. Immunological analysis of the activity of mitogen-activated protein kinase, ERK1/2, showed that this activity is up-regulated by ionizing radiation. These results suggest that ERK1/2 pathway is involved in the up-regulation of VEGF expression ionizing radiation mediated by AP-1, which may lead to further neovascularization and proliferation of glioblastoma cells resistant to radiation therapy.

Blotting, Northern↗
PubMed1975

Characteristics of histocompatibility barriers in congenic strains of mice. III. Passive enhancement of skin allografts in X-irradiated hosts.

Passive immunological enhancement of skin allografts was investigated in three donor-host combinations of congenic mice disparate at non-H-2 loci. Serum against the graft donor was derived from mice that had received donor strain lymphoid cells as neonates, and thereby were rendered specifically tolerant of a skin allograft. We refer to this serum as "allograft-tolerant" serum. Each strain combination was chosen to provide only two non-H-2 histoincompatibilities present in the donor and absent in the host. The differences are categorized as immunogenetically strong, moderate, or weak, on the basis of skin allograft survival times. With passively administered allograft-tolerant serum significantly prolonged graft survivals were noted for the weakest combination only. Combined treatment with sublethal X-irradiation and allograft-tolerant serum signigicantly prolonged graft survivals were noted for the weakest combination only. Combined treatment with sublethal X-irradiation and allograft-tolerant serum significantly prolonged graft survival in both the moderate and weak combinations, with the largest effect present in the weakest disparity. A hyperimmune alloantiserum (produced in adults) directed against the graft donor prolonged allograft survival in the strongest disparity when given in combination with irradiation. In this combination, graft survival time was increased in hosts exposed to X-ray alone, but joint treatment with X-ray and the alloantiserum gave the largest increment. In contrast, combined treatment with the serum and an antithymocyte alloantiserum did not affect graft survival times. Treatment with both radiation and antithymocyte serum did not prolong graft survival beyond that in mice given only X-radiation. Immunological enhancement with central inhibition is assumed as the mechanism underlying prolonged graft survival, and it is suggested that a population of thymus-derived "killer" cells, sensitive to X-irradiation, is required for normal graft rejection.

Animals↗
PubMedDate not supplied

[Radiation and immunity. Contemporary view of old problems].

Some key problems of radiation immunology which were formulated during last decades have been considered. The possibility or their decision appeared at recent time proceeding from the new view on the ionizing irradiation as a source of biologically significant signals. From that point of view some experimental data concerning radiation effects on the maturation and selection of lymphocytes, contact interaction of immune system cells and cytokine network were reviewed. It was concluded that the disturbances of the spatial and temporary organization and integrative functions of immune system were the results of the non-adequate radiation-induced signalling.

Animals↗
PubMed2002

Neoadjuvant and adjuvant therapy for resectable hepatocellular carcinoma: review of the randomised clinical trials.

Hepatocellular carcinoma (HCC) is common worldwide, and its incidence is increasing. Liver resection or transplantation is potentially curative, although subsequent recurrence and death are common. We reviewed randomised trials on the role of adjuvant therapy in resectable HCC. We identified 13 randomised trials with recurrence or survival endpoints reported at 3 years or longer. Three studies involved predominantly systemic adjuvant chemotherapy; four involved predominantly hepatic-artery-based chemotherapy or embolisation; and six used other therapeutic modalities including immunological, radiation, and differentiation agents. A therapeutic benefit in terms of disease-free or overall survival was noted in six trials, five of which involved modalities other than systemic or hepatic-artery chemotherapy or embolisation. We conclude that systemic and hepatic-artery chemotherapy or chemoembolisation have not been shown to improve overall or disease-free survival after resection of HCC, although there has been no definitive trial comparing adjuvant systemic chemotherapy with no treatment. Other adjuvant modalities (mostly tested in small, preliminary settings) may confer benefit after potentially curative resection of HCC.

Carcinoma, Hepatocellular↗