Die Vorhofseptumdefekte

Gleichmann, U; Loogen, F; Seipel, L

doi:10.1007/978-3-662-11977-8_16

Cited by 2 publications

(5 citation statements)

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“…The available recent evidence [7, 151 demonstrates that lethal GVH disease correlates with the capacity of C57BU10 parental T cells to generate suppression. Additional studies support the immunosuppression concept, both in mice [ 1 4 , 16-20] and in humans [21, 221. In contrast, D2 parental T cells are able to generate help rather than suppression, which results in a generalized B cell immunostimulation leading to autoimmune disease resembling systemic lupus erythematosus (SLE) [7]. Recent experiments favor the hypothesis that the autoantibodies characteristic of SLE are induced by abnormal T-B cell cooperation across the I-E subregion of the major histocompatibility complex [23].…”

Section: Discussionmentioning

confidence: 99%

“…A GVH index of 1.3 or greater was considered positive. (7) D2 (7) Two transfers 2 weeks apart. At the time of the second transfer, B6D2Fl recipients were 10 weeks old.…”

Section: Evaluation Of Gvh Diseasementioning

confidence: 99%

“…In addition, this species is of particular interest in several disease models studying experimental autoimmune myasthenia gravis [4] or immunity to infectious agents such as treponema [5] and cholera [6]. In recent years the availability of rabbits identical at the major histocompatibility locus has allowed transplantation research in noninbred animals [7]. blood leukocytes PBS: Phosphate-buffered saline PHA: Phytohemagglutinin PWM: Pokeweed mitogen R~M I~: Rabbit antimouse Ig sIg: Surface Ig TRITC: Tetramethylrhodamine isothiocyanate Despite its potential, the Use Of the rabbit as an experimental animal is, however, hampered by the poor characterization of its non-Ig lymphocyte surface markers.…”

Section: Rabbit Leukocyte Surface Antigens Defined By Monoclonal Antimentioning

confidence: 99%

“…Since it has been reported that both acute and chronic murine graft-vs. -host (GVH) [ 13 disease is associated with generalized immunodepression [14] and, in some strain combinations, is further associated with the development of malignant lymphoma [5-71 and autoimmune disease [7], we deemed it important to analyze natural killer (NK) activity in mice undergoing GVH reactions. It has been previously reported that (C57BL/6 x DBA/2)F1 hybrids (B6D2F1) receiving varying doses of C57BW6 (B6) parental spleen cells (SC), in quantities sufficient to provoke a positive GVH reaction, developed an increased incidence of malignant lymphoma [5], as compared to the syngeneic-injected controls.…”

Section: Introductionmentioning

confidence: 99%

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Natural killer activity in (C57BL/6 × DBA/2)F₁ hybrids undergoing acute and chronic graft‐vs.‐host reaction

et al. 1983

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The present findings demonstrate that a total i.v. transfer of 100 X 10(6) C57BL/6 (B6) parental spleen cells into untreated (C57BL/6 X DBA/2)F1 hybrids (B6D2F1) resulted in acute runting, which was associated with a significantly elevated graft-vs.-host (GVH) index over a one-month period following GVH induction. Furthermore, this B6-induced acute GVH disease was associated with a marked depression of natural killer (NK) cell activity (spleen and peripheral blood) (with or without addition of mouse fibroblast interferon), which correlated with lymphoid cell hypocellularity, prominent splenic extramedullary hematopoiesis (EMH), and parallel depressions of both concanavalin A- and lipopolysaccharide-induced mitogenesis. Significantly increased killing by antibody-dependent cellular cytotoxicity of antibody-coated chicken red blood cells, as well as increased T cell killing of the NK-insensitive cell line P815 (as compared to the significantly decreased killing of the NK-sensitive cell line YAC-1) was also observed in the spleens of this 100 X 10(6) B6-injected F1 group. In marked contrast to this 100 X 10(6) B6-injected acute GVH group, untreated mice injected i.v. with the same or greater numbers of parental DBA/2 spleen cells (100 X 10(6)-150 X 10(6) DBA/2 spleen cells) exhibited a milder and more chronic form of GVH disease, which was not associated with a significant decrease of NK activity. It was of considerable interest that a total i.v. transfer of 50 X 10(6) B6 spleen cells (i.e. one-half of that required to produce acute GVH, markedly depressed NK, and prominent splenic EMH) into B6D2F1 hybrids also resulted in a more chronic form of GVH disease, but was associated with significantly increased levels of NK activity at two weeks post GVH induction.

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Section: Discussionmentioning

confidence: 99%

“…A GVH index of 1.3 or greater was considered positive. (7) D2 (7) Two transfers 2 weeks apart. At the time of the second transfer, B6D2Fl recipients were 10 weeks old.…”

Section: Evaluation Of Gvh Diseasementioning

confidence: 99%

Section: Rabbit Leukocyte Surface Antigens Defined By Monoclonal Antimentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Natural killer activity in (C57BL/6 × DBA/2)F₁ hybrids undergoing acute and chronic graft‐vs.‐host reaction

et al. 1983

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“…In order t o determine the relative proportions of donor cells, host cells, and T cells in the spleens of GVH animals, their cells were typed by the cytotoxic test, a method known to give highly reliable results under comparable experimental conditions [ 14,18,191. The results indicate that virtually all cells detectable by this method, i.e.…”

Section: Determination Of Donor and Host Cellsmentioning

confidence: 99%

Diseases caused by reactions of T lymphocytes to in compatible structures of the major histocompatibility complex. I. Autoimmune hemolytic anemia

Gleichmann

1976

Eur J Immunol

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Diseases caused by reactions of T lymphocytes to in com pat i ble structures of the major h istocom pa t i b i I i t y complex 1. Autoimmune hemolytic anemia"The capacities of various lymphoid cells from C57BL/10 donors t o induce antibodies against red blood cells (RBC) in (C57BL/10 x DBA/2)Fl recipients were compared: cortisone-resistant thymocytes were more potent inducers than spleen cells, and bone marrow cells were ineffective. This established a need for parental T lymphocytes in the induction of Coombs-positive hemolytic anemia by the graft-versus-host reaction (GVHR). Since some of the anti-RBC antibodies carried the Igc allotype specific for the F1 host, they were autoantibodies.When antibodies were eluted from the erythrocytes of F1 mice undergoing the GVHR (GVH F l mice) and subsequently tested against normal RBC in the indirect Coombs' test, the Igc allotype was demonstrable even on those antibodies found t o react with RBC of the donor strain (C57BL/10). In addition, reactions with normal intact RBC of other strains and species were noted. Anti-RBC antibodies belonged t o all Ig classes and subclasses that were tested (IgG1, k G z a , k G z b , IgA, and IgM).By means of histocompatibility typing it was shown that the overwhelming majority of lymphoid cells from GVH animals were host cells; most of these host cells were Thy-1.2-negative. In several GVH F1 mice Coombs-positive erythrocytes were demonstrated for periods of more than 5 months; Igc-positive anti-RBC antibodies were detected for periods up t o 3 months. When an additional injection of parental T cells was administered t o GVH F1 mice, which had become Coombs-negative in the course of the GVHR, new anti-RBC antibodies appeared. In contrast t o F 1 B cells, T cells of the F1 host were not needed for autoimmunization as shown by the induction of anti-RBC autoantibodies in F1 recipients that were depleted of autologous T cells prior t o the administration of parental T cells.When (C57BL/10 x DBA/2)Fl mice were back-crossed into strain C57BL/10 and the offsprings injected with C57BL/10 (H-2bb) lymphoid cells, most of the H-2 heterozygous (H-2bd) back-crosses developed Coombs'-positive hemolytic anemia, whereas none of the H-2 homozygous (H-2bb) ones did.The most likely explanation of these results is that anti-RBC autoantibodies were induced by a persistent reaction of parental T helper cells to incompatible H-2 structures on normally present autoreactive F l B cells. The hypothesis is proposed that reactions of T lymphocytes against virally or chemically altered structures of the major histocompatibility complex may lead t o autoimmunization also in nonchimeric individuals.

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Die Vorhofseptumdefekte

Cited by 2 publications

References 218 publications

Natural killer activity in (C57BL/6 × DBA/2)F₁ hybrids undergoing acute and chronic graft‐vs.‐host reaction

Natural killer activity in (C57BL/6 × DBA/2)F₁ hybrids undergoing acute and chronic graft‐vs.‐host reaction

Diseases caused by reactions of T lymphocytes to in compatible structures of the major histocompatibility complex. I. Autoimmune hemolytic anemia

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Die Vorhofseptumdefekte

Cited by 2 publications

References 218 publications

Natural killer activity in (C57BL/6 × DBA/2)F1 hybrids undergoing acute and chronic graft‐vs.‐host reaction

Natural killer activity in (C57BL/6 × DBA/2)F1 hybrids undergoing acute and chronic graft‐vs.‐host reaction

Diseases caused by reactions of T lymphocytes to in compatible structures of the major histocompatibility complex. I. Autoimmune hemolytic anemia

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Natural killer activity in (C57BL/6 × DBA/2)F₁ hybrids undergoing acute and chronic graft‐vs.‐host reaction

Natural killer activity in (C57BL/6 × DBA/2)F₁ hybrids undergoing acute and chronic graft‐vs.‐host reaction