Chronic Allogeneic Disease

Lewis, Robert M.; Armstrong, Martine Y. K.; André-Schwartz, J; Müftüoğlu, A U; Beldotti, Lorraine; Schwartz, Robert S.

doi:10.1084/jem.128.4.653

Cited by 74 publications

(20 citation statements)

References 34 publications

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“…A nonimmunologic event occurring as a result of the administration of parental spleen cells to FI hybrids seems an unlikely cause of the nephritis because inactivation of the donor cells by mitomycin, or the administration of immunoincompetent cells (liver cells) does not cause nephritis (2). Additional evidence directly incriminating the donor cell as the initiator of the events leading to glomerulonephritis is provided by the dose-response curve shown in Fig.…”

Section: Discussionmentioning

confidence: 83%

“…Histopathology.--Kidneys were fixed in 10% buffered formalin and stained with periodic acid-Schiff (PAS). Immunofluorescent and electron microscope studies were carried out by previously described methods (2). Glomerulonephritis was diagnosed when any two of the following abnormalities were found: at least 300 mg/100 ml of protein in the urine, glomerular lesions identifiable by light microscopy, or deposits of immunoglobulins on the glomerular basement membranes when the kidney was examined by the immunofluorescent technic.…”

Section: Methodsmentioning

confidence: 99%

“…Spleen Cell Suspensions.--A previously described technic was used (2). Histopathology.--Kidneys were fixed in 10% buffered formalin and stained with periodic acid-Schiff (PAS).…”

Section: Methodsmentioning

confidence: 99%

“…In three of these cases the cells of an H-2 a parent were injected into a hybrid possessing the H-2 b allele. In the fourth example, HTG cells were injected into (C57BL/6 X HTG)F1 hy- 2 Hybrids in which one parent was H-2 d and the other H-2 b did not, however, invariably develop glomerulonephritis, the incidence varying from 0 % to 87.3 %.…”

Section: The Ability Of Spleen Cells From Different Inbred Mice To Inmentioning

confidence: 99%

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Chronic Allogeneic Disease

Gleichmann

André-Schwartz

et al. 1972

The Journal of Experimental Medicine

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The pathogenesis of glomerulonephritis in F1 hybrid mice injected with parental spleen cells was investigated in several ways. Whenever glomerulonephritis developed, the lesion had the typical morphology produced by antigen-antibody complexes. Experiments employing backcross mice demonstrated that the antigen is supplied by the recipient and that it is specified by the H-2 gene complex, or by a locus closely linked to H-2. The source of the antibody was investigated by staining glomerular lesions with fluorescein isothiocyanate-tagged anti-immunoglobulin allotype sera. Only donor-type allotypes could be detected. The ability of the donor's immunocytes to respond to the recipient's histocompatibility antigens in such a way as to produce nephritogenic immune complexes varied from strain to strain, and seemed to be controlled by a gene unrelated to H-2. The results suggest that cell surface antigens, such as histocompatibility antigens, may be of importance in the pathogenesis of several kinds of glomerulonephritis.

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Section: Discussionmentioning

confidence: 83%

Section: Methodsmentioning

confidence: 99%

“…Spleen Cell Suspensions.--A previously described technic was used (2). Histopathology.--Kidneys were fixed in 10% buffered formalin and stained with periodic acid-Schiff (PAS).…”

Section: Methodsmentioning

confidence: 99%

Section: The Ability Of Spleen Cells From Different Inbred Mice To Inmentioning

confidence: 99%

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Chronic Allogeneic Disease

Gleichmann

André-Schwartz

et al. 1972

The Journal of Experimental Medicine

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“…The stained sections were graded on a 0-4+ scale by estimating both the brightness and the extent of fluorescent staining (18). In addition to an overall score for the entire glomerulus, separate scores were assigned to the mesangium and capillary loops.…”

Section: Immunofluorescence Of Kidney Sectionsmentioning

confidence: 99%

Genetic studies of autoimmunity and retrovirus expression in crosses of New Zealand black mice I. Xenotropic virus.

Datta

Manny

Andrzejewski

et al. 1978

The Journal of Experimental Medicine

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Type C RNA viruses (retroviruses) have been implicated in the autoimmune disease of New Zealand Black (NZB) 1 mice (1, 2). However, the evidence for this is only circumstantial because the retroviruses isolated from NZB mice are xenotropic in host range; this prohibits a direct test of their pathogenicity in mice by, for example, inoculation of filtrates (3, 4). Nevertheless, the relationship between autoimmunization and xenotropic viruses c&n be ascertained by genetic tests because the genes of these agents are an integral part of cellular chromosomes (5) and their expression in NZB mice is governed by two autosomal dominant genes (6, 7). In this paper we describe results of genetic experiments designed to test the hypothesis that expression of xenotropic virus is required for the development of autoimmune disease. The following paper (8) deals with the relationship between autoimmune disease in NZB mice and expression of the major envelope glycoprotein of the virus, gp70. Materials and MethodsMice. NZB, SWR, C57BL/6, B10.A, and AKR mice were obtained from The Jackson Laboratory, Bar Harbor, Maine. Reciprocal crosses were made to produce FI and backcross progeny mice. Because the maternal direction of the cross did not affect the results, all data for a given cross were pooled and presented by a single nomenclature: F~ for (SWR × NZB)F~; (F~ × SWR) for backcross to SWR, and (F~ x NZB) for backcross to NZB. The mice were 11-24 mo old when tested.Retrovirus Assays XI~.NOTROPIC VIRUS. Spleen cell suspensions were prepared and serially diluted as described previously (6, 7, 9). They were assayed by cocultivation on monolayers of the feline 81 cell line

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Immunologic activation of murine leukemia viruses

Melief

Datta

Louie

et al. 1974

Cancer

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We propose that neoplasms of lymphoid tissue arise, not as a result of immunosuppression, but as a consequence of immunostimulation. Evidence from experimental models and clinical findings is marshalled in favor of this idea. Unchecked immunostimulation may lead to activation of latent oncogenic viruses, which in turn transform lymphoid cells to a malignant state. The feedback control of the immune response may keep the activation mechanism in check; if this is so, deregulation of the immune response would favor activation of oncogenic viruses and hence the development of malignant lymphoproliferative diseases.

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Chronic Allogeneic Disease

Cited by 74 publications

References 34 publications

Chronic Allogeneic Disease

Chronic Allogeneic Disease

Genetic studies of autoimmunity and retrovirus expression in crosses of New Zealand black mice I. Xenotropic virus.

Immunologic activation of murine leukemia viruses

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