Generation of biliary lesions after transfer of human lymphocytes into severe combined immunodeficient (SCID) mice.

Krams, Sheri M.; Dorshkind, Kenneth; Gershwin, M. Eric

doi:10.1084/jem.170.6.1919

Cited by 173 publications

(91 citation statements)

References 23 publications

(29 reference statements)

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“…The scid mouse is also used in a number of other experimental models of human disease, e.g. autoimmune and allergic diseases [14,15]. Our interest for the scid mouse in the present study was as an immunologically impaired primary tumour host.…”

Section: Introductionmentioning

confidence: 99%

MCA Sarcomas Induced in scid Mice are More Immunogenic than MCA Sarcomas Induced in Congenic, Immunocompetent Mice

et al. 1997

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Engel A-M, Svane IM, Rygaard J, Werdelin O. MCA Sarcomas Induced in scid Mice are More Immunogenic than MCA Sarcomas Induced in Congenic, Immunocompetent Mice. Scand J Immunol 1997;45:463-470 With the aim of studying possible T-cell mediated selection of the cells in growing tumours, 108 mice of the C.B-17 strain, either immunocompetent C.B-17 mice or histocompatible immunodeficient C.B-17 severe combined immune deficiency (scid) were treated with 3-methylcholanthrene (MCA) in two different dosages. A total of 51 tumours were obtained, 44 of which were established as uncloned tumour cell lines, and used for further study. Tumour incidence correlated with carcinogen-dosage in that more tumours developed in groups treated with a high MCA dose than in groups treated with a low MCA dose, but not with immune status of the tumour host. No significant difference in the level of MHC class I molecule expression was found between the two groups of tumours. The rate of rejection after transplantation to syngeneic immunocompetent hosts was significantly higher for the scid tumours than for the non-scid tumours. The authors suggest that this reflects an immunoselection performed by T cells in the immunocompetent host in which the tumour originated, which has eliminated highly immunogenic tumour cells, leaving non-immunogenic tumour cells to grow.

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Section: Introductionmentioning

confidence: 99%

MCA Sarcomas Induced in scid Mice are More Immunogenic than MCA Sarcomas Induced in Congenic, Immunocompetent Mice

et al. 1997

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“…There were also degenerative changes in or destruction of bile ducts, but similar pathology was found in some SCID mice reconstituted with normal hu-PBL, and it is apparent that these histopathological changes were due to GVHD [10]. An increase in dermal collagen in more than 80% of skin surface area was shown in all SCID mice that received hu-PBL from patients with scleroderma, but also in 1/4 of recipients of hu-PBL from normal donors [12]; however, this is a pathologic feature of human chronic GVHD [30].…”

Section: Tissue Damagementioning

confidence: 85%

“…Some autoantibodies (e.g. AMA and ANA) were detected up to 7 months post-engraftment [12,27], and anti-human TPO have been shown in SCID mice 119 days after grafting hu-PBL [28]. It is not clear whether (auto)antibodies to certain antigens persist longer than those to other antigens and, if this is the case, whether the cross-reactivity between mouse and human antigens is of importance in this respect.…”

Section: Autoantibodiesmentioning

confidence: 92%

“…lymphokines and cell adhesion molecules) for the function of human T lymphocytes. There are reports of GVHD that occurs after injection of hu-PBL [12], although most investigators did not find GVHD after this injection. Unsterile conditions (only a few reports mentioned the prophylactic use of antibiotics [16]) can lead to activation of NK cells, leakiness of SCID mice, and GVHD.…”

Section: Pitfalls and Importance Of The Scid Mouse Model Of Autoimmunitymentioning

confidence: 99%

“…Human T lymphocyte unresponsiveness can occur because ofthe absence of autologous APC that provide costimulatory signals required for T lymphocyte activation. The human T lymphocytes from hu-PBL engrafted to SCID mice do not produce gr&it-versus-hosX disease (GVHD) according to some researchers [11], but may show evidence of GVHD according to other investigators [12,13]. Leakiness is associated with GVHD and sporadic GVHD might be explained by variations in natural killer (NK) activation.…”

Section: Scid Micementioning

confidence: 99%

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Untitled

1993

Clinical &Amp; Experimental Immunology

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SUMMARYThere are no readily available in vivo models to study immune cells from humans with autoimmune diseases. SCID mice, which virtually lack both T and B lymphocytes and accept xenogeneic cells, have been used during the last 5 years to provide a milieu for lymphocytes isolated from individuals with various autoimmune diseases, or for lymphocytes from mice that have a systemic lupus erythematosus-like syndrome. Whilst human autoantibodies to organ antigens have been demonstrated in most SCID mice engrafted with human lymphocytes from the peripheral blood or the target organ, inflammation ofthe mouse target organ has not generally been observed. This review critically analyses experiments in this area reported so far. Some pitfalls ofthe SCID mouse model of human autoimmune diseases are mentioned, and future experiments to study mouse and human autoimmunity with this model are proposed.

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Human T-cell lymphotropic virus type-I infection in the severe combined immunodeficiency mouse

et al. 1996

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Human T-cell lymphotropic virus type-I (HTLV-I) is the etiologic agent of HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and adult T-cell leukemia (ATL). HAM/TSP and ATL occur infrequently among HTLV-I-infected individuals, and rarely develop in the same individual. To study host and viral factors involved in the induction, tissue tropism, as well as pathogenesis of HAM/TSP, peripheral blood lymphocytes (PBL) from 14 patients with HAM/TSP and from 9 controls were introduced into severe combined immunodeficiency (SCID) mice by intraperitoneal injection. Mice were followed for up to 26 weeks. Human IgG was produced from 2 to 14 weeks after reconstitution in all animals. Thirty-two of 44 mice (72%) showed circulating human antibody against the major viral protein products of HTLV-I. Analysis of viral sequences by polymerase chain reaction (PCR) demonstrated HTLV-I sequences in 21/38 (55%) brains and in 7/17 (41%) spinal cords from HTLV-I-hu SCID mice. No animal had clinical evidence of neurological impairment or pathological findings similar to those seen in HAM/TSP. Seven mice who received PBL from Epstein Barr virus (EBV)-seropositive patients developed an intraperitoneal lymphoma. In 2 mice an infiltration of brain by a lymphoblastic tumor of B/T cell type was observed. By PCR, all the tumors were EBV-positive; HTLV-I sequences were detected in 5 of them. Our study suggests that the HTLV-I-hu-SCID mouse provides a potentially valuable system for studying the production, kinetics, and pathogenicity of anti-HTLV-I antibody, and may help clarify the interaction of EBV and retroviruses in the development of disease.

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Generation of biliary lesions after transfer of human lymphocytes into severe combined immunodeficient (SCID) mice.

Cited by 173 publications

References 23 publications

MCA Sarcomas Induced in scid Mice are More Immunogenic than MCA Sarcomas Induced in Congenic, Immunocompetent Mice

MCA Sarcomas Induced in scid Mice are More Immunogenic than MCA Sarcomas Induced in Congenic, Immunocompetent Mice

Untitled

Human T-cell lymphotropic virus type-I infection in the severe combined immunodeficiency mouse

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