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PubMed1991

Limited B cell repertoire in severe combined immunodeficient mice engrafted with peripheral blood mononuclear cells derived from immunodeficient or normal humans.

The ability to engraft human PBMC or fetal tissue immune cells in the severe combined immunodeficient (SCID) mouse has created a need for characterization of these systems and their application to disease models. We demonstrate that SCID mice reconstituted with PBMC support the growth and differentiation of a restricted set of B cells. Human IgG levels of 1-2 mg/ml (10-20% of normal human serum levels) were routinely achieved in spite of a serum half life of only 12 d. Ig levels peaked around 50 d and Ig production was maintained for greater than 100 d. The Ig was greater than 85% IgG though some IgM, IgA, IgD, and even IgE could be detected. However, the human IgG produced in hu-PBL-SCID mice was pauci-clonal when analyzed by isoelectric focusing and by kappa/lambda light chain usage. Using a new polymerase chain reaction based analysis capable of monitoring individual VH family utilization, we found that the engrafted B cells showed skewed and restricted human VH subfamily utilization. These parameters were markedly variable among hu-PBL-SCID mice reconstituted from the same donor cell population at both early (21-50 d) and late stages (greater than 100 d). Hu-PBL/CVI-SCID mice constructed with cells from patients with common variable immunodeficiency with an in vitro block in terminal B cell differentiation produced human Ig responses that were quantitatively the same as those produced by hu-PBL-SCID mice from normal donors. The hu-PBL-SCID system using PBMC appears to lead to growth and Ig production by a small number of B cells and results in a restricted B cell repertoire.

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PubMed1992

Human peripheral blood lymphocytes transplanted into SCID mice constitute an in vivo culture system exhibiting several parameters found in a normal humoral immune response and are a source of immunocytes for the production of human monoclonal antibodies.

Human PBL from vaccinated healthy blood donors, which was transplanted i.p. into mice with severe combined immunodeficiency (SCID), exhibited an Ag-dependent humoral Ir against tetanus toxoid. This Ir was dose dependent and was completely abrogated by immunizing with large amounts of Ag, suggesting a high dose tolerization of the B cells. A dose-dependent selection of specific, high affinity B clonotypes was also suggested, since immunization with low concentrations of tetanus toxoid produced antisera with higher avidity than immunizations using a high dose of Ag. The production of human Ig and the clonal outgrowth of normal human B cells in the SCID mouse was strongly down-regulated by human NK cells. Human immune B lymphocytes were also recovered from immunized SCID mice and transformed with EBV, yielding lymphoblastoid cell lines producing high affinity antitetanus human IgG antibodies. These results suggest that SCID mice, repopulated with human PBL, can constitute a functional model of several parameters of a normal human humoral Ir and can provide a source of immune B cells for the production of human mAb.

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PubMed1995

Antigen-presenting cells for naive transgenic gamma delta T cells. Potent activation by activated alpha beta T cells.

The function of gamma delta T cells, particularly the minor population of circulating gamma delta T cells, remains unclear. To study these lymphoid gamma delta T cells, a transgenic SCID mouse containing the KN6 gamma delta TCR whose ligand is the TL gene product, T22b, was created. KN6-SCID mice contain a monoclonal population of naive KN6+ gamma delta T cells. Using these mice, we have studied the APC required for activation of KN6+ gamma delta T cells in vitro and in vivo. Analysis of an in vitro mixed lymphocyte response identified a hierarchy of potency for stimulation: dendritic cells = T cell blasts > B cell blasts > B cells > resting T cells. In contrast, in vivo, only alpha beta T cells fully activated KN6+ gamma delta T cells as measured by an increase in the number of splenic KN6+ cells, the development of blast morphology, and the development of proliferative anergy in the responding KN6+ cells. The strong stimulatory properties of C57BL/6J T cells appeared to depend on their having been activated by KN6-SCID alloantigens. T cells from (C57BL/6J x BALB/c)F1 mice, which are tolerant of KN6-SCID alloantigens, could not fully activate KN6+ cells. However, the F1 T cells could activate KN6+ cells if they were activated in vivo by the mitogen, staphylococcal enterotoxin B. A mixture of third party activated T cells plus T22b+ non-T cells only partially activated KN6+ cells, implying that activated T22b+ T cells are acting directly as stimulatory cells. Although the Ags recognized by gamma delta T cells are generally unknown, Ag presentation by activated alpha beta T cells may be an important method of activation.

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PubMed1997

Use of immunodeficient mice in metastasis research.

One of the major clinical problems facing the western world is how to stem the tide of deaths from metastasising malignancies. Despite some progress in diagnosis and treatment, the death rate from major clinically important tumours, such as lung, breast and colon cancer, shows no signs of abating. This therapeutic failure is due to tumour metastasis, for which no treatment options are available. Effort has been made to find valid animal models in which the metastatic process can be studied, and in which putative treatments can be evaluated. This review discusses some of the approaches used in creating these models, and focuses on current work using the severe combined immunodeficient (SCID) mouse.

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PubMed2005

In vivo antitumor activity of the NF-kappaB inhibitor dehydroxymethylepoxyquinomicin in a mouse model of adult T-cell leukemia.

Adult T-cell leukemia (ATL) is an aggressive neoplasm caused by human T-cell leukemia virus type I (HTLV-I). The nuclear transcription factor, NF-kappaB, is induced by HTLV-I and is central to the ensuing neoplasia. To examine the effect of a novel NF-kappaB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on ATL in vivo, we developed an improved severe combined immunodeficiency (SCID) mouse model for ATL. Five-week-old SCID mice in which natural killer (NK) cell activity had been eliminated were inoculated intraperitoneally with the HTLV-I-infected cell lines, TL-Om1, MT-1, MT-2 and HUT-102. No engraftment of TL-Om1 cells and little tumorigenesis of MT-1 cells were detected 40 days after injection. In contrast, inoculation of mice with MT-2 and HUT-102 cells elicited high mortality, 100% frequency of gross tumor formation and tumor cell infiltration of various organs, all of which were reduced by coadministration of DHMEQ during the inoculation. Moreover, tumors from mice treated with DHMEQ had a high frequency of apoptosis. These results suggest that DHMEQ induces apoptosis in HTLV-I-transformed cells in vivo, resulting in inhibition of tumor formation and organ infiltration, thereby enhancing survival.

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PubMed1993

A study on the engraftment and trafficking of bovine peripheral blood leukocytes in severe combined immunodeficient mice.

Bovine lymphoid cells were engrafted into untreated and into sublethally irradiated scid/scid mice, following intraperitoneal (i.p.) injection of bovine peripheral blood leukocytes (PBL). To distinguish bovine from murine cells, bovine PBL were stained prior to i.p. injection with a fluorescent cell linker compound, PKH26-GL and, after cell recovery, labelled with a monoclonal antibody (mAb) reactive with the bovine pan leukocyte cell surface marker, CD45, and analyzed by flow cytometry. This dual labelling system was used to monitor tissue localization and migration of bovine cells within PBL-SCID-bo from 30 min to 64 days after bovine PBL injection. Inoculated bovine PBL were rapidly cleared from the peritoneal cavity of PBL-SCID-bo over the first 24 h after injection, then bovine cell numbers within the peritoneal cavity increased gradually over the next 35 days. No bovine cells were observed in the peritoneal wash from either non-irradiated or irradiated mice after Day 56. Bovine cells were detected in the spleens of both non-irradiated and irradiated mice 12-14 days after inoculation, but were undetectable in non-irradiated and irradiated mice after Day 56, and in irradiated mice after Day 35. This decrease coincided with a significant reduction in both the numbers of bovine cells in the peritoneal cavity, and in the levels of bovine Ig detected in the sera. Bovine IgG and bovine IgM were detected in both normal and irradiated PBL-SCID-bo by 4 days after PBL injection, and remained detectable to 8 weeks after inoculation. T-cells appeared to be the predominant bovine cell population in the spleens. In a small proportion of both normal and irradiated PBL-SCID-bo, spleens three to 20 times the size of a normal SCID mouse spleen were observed. Relatively high levels of bovine cells were detected in the thymuses of some irradiated PBL-SCID-bo. Sporadic, low levels of bovine cells were observed in the mesenteric lymph nodes, peripheral blood, and kidneys of normal and irradiated mice, and in the lungs and livers of non-irradiated but not irradiated PBL-SCID-bo. Sublethal gamma irradiation of SCID recipients appeared to enhance engraftment of bovine cells into the murine spleen and thymus.

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PubMed1995

Membrane-associated CD19-LYN complex is an endogenous p53-independent and Bc1-2-independent regulator of apoptosis in human B-lineage lymphoma cells.

CD19 receptor is expressed at high levels on human B-lineage lymphoid cells and is physically associated with the Src protooncogene family protein-tyrosine kinase Lyn. Recent studies indicate that the membrane-associated CD19-Lyn receptor-enzyme complex plays a pivotal role for survival and clonogenicity of immature B-cell precursors from acute lymphoblastic leukemia patients, but its significance for mature B-lineage lymphoid cells (e.g., B-lineage lymphoma cells) is unknown. CD19-associated Lyn kinase can be selectively targeted and inhibited with B43-Gen, a CD19 receptor-specific immunoconjugate containing the naturally occurring protein-tyrosine kinase inhibitor genistein (Gen). We now present experimental evidence that targeting the membrane-associated CD19-Lyn complex in vitro with B43-Gen triggers rapid apoptotic cell death in highly radiation-resistant p53-Bax- Ramos-BT B-lineage lymphoma cells expressing high levels of Bcl-2 protein without affecting the Bcl-2 expression level. The therapeutic potential of this membrane-directed apoptosis induction strategy was examined in a scid mouse xenograft model of radiation-resistant high-grade human B-lineage lymphoma. Remarkably, in vivo treatment of scid mice challenged with an invariably fatal number of Ramos-BT cells with B43-Gen at a dose level < 1/10 the maximum tolerated dose resulted in 70% long-term event-free survival. Taken together, these results provide unprecedented evidence that the membrane-associated anti-apoptotic CD19-Lyn complex may be at least as important as Bcl-2/Bax ratio for survival of lymphoma cells.

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PubMed1997

IL-10 inhibition of human prostate PC-3 ML cell metastases in SCID mice: IL-10 stimulation of TIMP-1 and inhibition of MMP-2/MMP-9 expression.

The molecular mechanism by which IL-10 inhibits metastases was examined using a SCID mouse model. Human PC-3 ML subclones normally metastasize to the lumbar vertebrae (approximately 70% mice injected, n = 14/20) following intravenous injection in severe combined immunodeficient (SCID) mice. IL-10 treatment of the PC-3 ML cells (15 ng/ml for 36 h) and the SCID mice (0.03 mg/kg/day for 30 days) reduced the number of metastases to 5% of the mice (n = 1/20). More importantly, following discontinuation of IL-10 treatment on day 30, the mice remained tumor-free and mouse survival rates increased dramatically (from < 30% in untreated mice) to about 85% in IL-10-treated mice. IL-10 did not appear to alter the growth rates or colony-forming ability of the PC-3 ML cells in vitro. Likewise, the growth of subcutaneous tumors and established bone marrow metastases was not inhibited by IL-10 treatment of the SCID mice. However IL-10 may inhibit the production of matrix metalloproteases (MMP) and prevent the establishment of metastasis. We therefore examined the influence of IL-10 on PC-3 ML production of MMP-2/MMP-9 and the tissue inhibitors of metalloproteinases (TIMP-1/2). Enzyme-linked immunosandwich assays (ELISAs) revealed that IL-10 (15 ng/ml for 36 h) treatment of the PC-3 ML cells down-regulated MMP-2 and MMP-9 while up-regulating TIMP-1 (not TIMP-2) expression. Likewise, IL-10-treated mice exhibited similar changes in TIMP-1 and MMP-2/MMP-9 expression. The IL-10 effects were blocked by IL-10 receptor antibodies. In comparison to IL-10, IL-4 failed to influence metastasis or the expression of TIMP-1, TIMP-2, MMP-2 and MMP-9 by PC-3 ML cells. We suggest that IL-10-regulated increases in the molar ratio of TIMP-1/MMP-9 and TIMP-2/MMP-2 might inhibit processes critical to the establishment of bone marrow metastasis.

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PubMed1996

The scid mutation does not affect slowly repairing potentially lethal damage that is sensitive to 0.23 M NaCl.

The repair of slowly repairing potentially lethal damage (PLD) in radiosensitive cells from the severe combined immunodeficient (scid) mouse was compared with that in Balb/c 3T3 cells with "wild-type" radiosensitivity and that in RD13B2 cells derived from scid cells whose sensitivity is normal because of the presence of fragments of human chromosome 8. Treatment with 0.23 M NaCl was used for fixation of slowly repairing PLD. The scid cells repaired PLD sensitive to 0.23 M NaCl to a great extent whin 3-4 h, similarly to Balb/c 3T3 and RD13B2 cells. This indicates that the scid mutation hardly affects the repair of PLD sensitive to 0.23 M NaCl. On the other hand, as reported previously, the rapidly repairing PLD that is sensitive to 0.5 M NaCl was repaired only slowly (3-4 h) in scid cells, in contrast to the rapid repair (within 1 h) seen with Balb/c 3T3 and RD13B2. This suggests that scid mutation is responsible for this repair at reduced rate. To confirm the independence of repair of 0.23 M NaCl-sensitive PLD from that of 0.5 M NaCl-sensitive PLD, both treatments with 0.23 M NaCl and 0.5 M NaCl were combined in each line. It is found that the repair of either PLD was not affected by the other treatment. The scid mutation impaired only the repair of 0.5 M NaCl-sensitive PLD.

3T3 Cells↗

PubMed2003

Bone marrow reconstitution as a relevant model of genetically programmed leukemia.

Mouse model systems which allow bone marrow reconstitution can be used to analyse genetically programmed leukemia. The original and most widely used system is that of post 5-fluorouracil mouse hematopoietic stem cells (HSC) into lethally irradiated syngeneic mice. Another more recent system allows analysis of human HSCs in the NOD-SCID mouse. Both systems are discussed as models for analysis of gene induced leukemia.

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PubMed2005

Concurrent administration of granulocyte colony-stimulating factor or granulocyte-monocyte colony-stimulating factor enhances the biological activity of rituximab in a severe combined immunodeficiency mouse lymphoma model.

A predominant percentage of the in vivo antitumor activity of rituximab occurs through antibody-dependent cellular cytotoxicity (ADCC) via FcgammaRIII receptors. Co-expression of CD11b/CD18 (MAC-1), an adhesion molecule present in activated neutrophils, plays an important role in the induction of ADCC. The effects of granulocyte-monocyte colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) on the biological activity of rituximab were studied in a non-Hodgkin's lymphoma (NHL)-bearing severe combined immunodeficiency (SCID) mouse model. Natural killer (NK) cell-depleted SCID mice were inoculated intravenously with Raji cells. Animals were divided into 6 cohorts: group A: placebo (saline injection); group B: murine (m)-G-CSF; group C: m-GM-CSF; group D: rituximab alone; group E: concurrent m-G-CSF and rituximab; and group F: concurrent m-GM-CSF and rituximab. Treatment with G-CSF or GM-CSF led to a 1.5- to 2-fold increase of CD11b/CD18 expression in neutrophils. Treatment with G-CSF led to the highest expression of CD11b/CD18 on neutrophils. No antitumor activity was observed among mice treated with G-CSF or GM-CSF alone. After 3 months, survival rates were highest in animals treated with rituximab and G-CSF (53.3%) compared to rituximab alone (13.3%) or in combination with peg-GM-CSF (26.7%). Increasing neutrophil counts via cytokine stimulation may play an important role in augmenting rituximab-associated antitumor activity.

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PubMed1998

Engraftment of human myelodysplastic syndrome derived cell line in transgenic severe combined immunodeficient (TG-SCID) mice expressing human GM-CSF and IL-3.

A transgenic SCID (TG-SCID) mouse expressing the human cytokines interleukin-3 (IL-3) and granulocyte-macrophage colony-stimulating factor (GM-CSF) has been generated with the aim of making a model system allowing the in vivo proliferation of human hematopoietic cells. Using TG-SCID mice expressing high levels (30-35 ng/ml in the serum) of human GM-CSF and IL-3, we attempted to engraft a human myeloid leukemia cell line, F-36P, derived from a myelodysplastic syndrome (MDS) patient. When F-36P cells were transferred intravenously into sublethally irradiated TG-SCID mice, extensive proliferation of F-36P cells was found 4-6 wk later. Successful engraftment, however, required the preadministration of a monoclonal antibody to mouse interleukin-2 receptor (IL-2R) beta chain, neutralizing NK activity. Surprisingly, all the transplanted TG-SCID mice engrafted with F-36P cells developed hind leg paralysis approximately 6 wk after transfer. Histological analysis demonstrated extensive invasion and formation of osteolytic lesions by the F-36P cells in the vertebrae. These data indicate that transgenic SCID mice expressing human IL-3 and GM-CSF provide a useful system for the study of human leukemia. In addition, NK cells appear to play an important role in rejection of human cells.

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PubMed1993

The diversity of in-frame TCR delta chain transcripts in aging SCID mice.

From spleen, liver, bone marrow, and gut of old C.B-17 scid/scid (SCID) mice, TCR delta chain transcripts were amplified by the polymerase chain reaction (PCR) using V delta 1-, V delta 2-, V delta 3-, V delta 4-, V delta 5-, V delta 6-, and C delta-specific primers. Selectively amplified, TCR delta-chain-encoding cDNA from these organs of five old SCID mice was cloned, and 175 randomly selected clones were sequenced. In this panel, 44 distinct rearrangement events were detected, 82% (36/44) of which were in-frame. For V delta 2, V delta 4, V delta 5, and V delta 6, 34 in-frame transcripts were found in five old SCID mice. No potentially functional transcript containing V delta 3 was found and an unusual type of transcript containing the V delta 1 gene segment spliced directly in-frame to C delta was the predominant type of V delta 1 expression. Junctional diversity was evident in most sequenced clones indicating an extensive potential diversity of SCID-derived TCR delta chains. Identical transcripts were amplified from different organs of the same old SCID mouse. No organ-specific expression of V delta genes was evident. TCR delta chain transcripts could be neither amplified from young SCID mice nor from young SCID mice nor from young or old scid/scid nu/nu mice (bred on a BALB/c background). Hence, an apparently thymus-dependent development of oligoclonal populations of TCR delta+ cells is observed in old SCID mice.

Aging↗

PubMed1985

The function of antigen-presenting cells in mice with severe combined immunodeficiency.

We have examined the antigen-presenting function of spleen cells in the C.B-17 scid mouse, a mutation that severely impairs the development of T and B lymphocytes. We show that antigen-presenting cells (APC) of SCID mice function normally in antigen-specific proliferative responses of primed T cells and in the antigen-specific activation of IL 2-producing T cell hybridomas. In both quantitative and qualitative terms, APC of SCID mice are equivalent to those of normal mice. These results indicate that the development and differentiation of APC function in vivo is independent of signals from mature, functional T or B lymphocytes.

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PubMed1996

Evidence for restricted diversity of antigen-specific human antibodies in immunized hu-PBL-SCID mice.

Previous studies have revealed that specific human humoral immune responses could be produced in immunized SCID mice after engraftment of human lymphocytes (hu-PBL-SCID). On the other hand, the engrafted repertoire of B cell clones is known to be skewed in hu-PBL-SCID with the corresponding production of only a limited set of major human antibodies. In this work, we have analyzed the diversity of tetanus toxoid-specific human antibodies produced in immunized hu-PBL-SCID mice in comparison with the total serum antibody population using zone electrophoresis followed by blotting. The results showed that the diversity of tetanus toxoid-specific antibody population was more restricted than that of the total human antibody population, with some animal sera containing a single band of tetanus toxoid-specific antibody molecule, in clear contrast to the polyclonal response of the PBL donor. Absorption experiments showed tetanus toxoid-specific antibodies could account for a significant proportion (up to 10%) of the total human antibodies present in hu-PBL-SCID mouse sera. The inability to expand a high number of different antigen-specific B cell clones in immunized hu-PBL-SCID mice represents an important intrinsic limitation of this animal model which may be caused by defects in T cell help.

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PubMed1998

Pathogenicity of Mycoplasma volis in mice and rats.

A new species of Mycoplasma, M. volis, was isolated from the respiratory tract of clinically normal field-trapped prairie voles (Microtus ochrogaster) that were to be housed in close proximity to other rodents. To determine the pathogenic potential of the new mycoplasmal isolate, three groups of rodents (Sprague Dawley rats, BALB/c mice, and severe combined immunodeficient [SCID] mice) were intranasally inoculated with 2 x 10(8) color-changing units (CCU) of M. volis and were observed for 4 to 6 weeks. Experimental animals did not manifest clinical signs of disease; however, one experimental SCID mouse was euthanized 5 days after inoculation because of a severe circling disorder. Lung lesions in experimental SD rats ranged from mild to severe bronchial-associated lymphoid tissue (BALT) hyperplasia. Lung lesions in BALB/c and SCID mice ranged from no lesions to mild pneumonia. We were able to isolate M. volis from some control mice, none of which had lung lesions. All mice were seronegative for Sendai virus, mouse hepatitis virus, and M. pulmonis. All immunocompetent experimental animals (BALB/c mice and Sprague Dawley rats) were seropositive for M. volis. All immunocompetent control animals and SCID mice were seronegative for M. volis. Our data suggest that M. volis is capable of causing microscopic lesions and seroconversion in rats and mice, and therefore these rodents should not be housed in close proximity to voles.

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PubMed2005

Dietary n-3 polyunsaturated fatty acids reduce disease and colonic proinflammatory cytokines in a mouse model of colitis.

BACKGROUND: n-3 polyunsaturated fatty acids (PUFAs) reduce the severity of chronic inflammatory bowel disease, probably by means of reduction of immune cell activation or enhancement of the epithelial barrier. Using the severe combined immunodeficient (SCID) mouse model of colitis, this study examined the effect of dietary n-3 PUFAs on development of colitis and on immunologic, epithelial, and matrix parameters in the intestines of control and colitic animals. METHODS: SCID mice were fed n-3-enriched or control diet for 3 weeks before colitis induction by transplantation of CD45RB T cells and maintained on the same diet for 4 to 8 weeks. Phenotype of infiltrating cells, epithelial ZO-1 protein, and mucosal type I collagen were assessed by immunohistology and tissue cytokines by ELISA. RESULTS: Transplanted n-3-fed animals had significantly reduced pathology scores, colonic tumor necrosis factor-alpha, interleukin-12, and interleukin-1beta compared with animals fed standard diet. Proinflammatory cytokines were reduced despite a similar level of immune cell infiltration by T cells, CD11c cells, and CD11b cells. Neutrophil infiltration was significantly reduced in n-3-fed control and colitic mice, and other myeloid populations were reduced in mice on the n-3 diet. Epithelial ZO-1 expression was increased, and myofibroblast activation significantly decreased in transplanted n-3-fed animals compared with standard diet mice. Submucosal collagen synthesis was enhanced in n-3-fed mice. CONCLUSIONS: Dietary n-3 PUFAs reduced clinical colitis and colonic immunopathology in this model of colonic inflammation by decreasing proinflammatory cytokine synthesis, reducing myeloid cell recruitment and activation, and enhancing epithelial barrier function and mucosal wound healing mechanisms.

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PubMed1997

Antibody isotype responses to Trichuris infection in humanized SCID mice.

We have developed a humanized SCID mouse model of trichuriasis involving the injection of peripheral blood lymphocytes (PBLs) from normal healthy donors into C. B. 17 severe combined immunodeficiency (SCID) mice followed by vaccination and infection of these mice with the murine species of Trichuris, Trichuris muris. Optimal results with respect to parasite specific antibody production and peripheral engraftment were achieved by injecting intraperitoneally 2 x 10(7) PBLs which had been incubated overnight on anti-human CD3 coated plates. Mice were immunized three weeks post reconstitution with parasite antigen in Freund's Incomplete Adjuvant and infected two weeks later. At autopsy human T cells could be detected in the spleens of engrafted animals and anti-T. muris antibody detected. The dominant IgG isotype responses were shown to be IgG1 and IgG2, providing a similar IgG isotype profile to that seen in humans infected with T. trichiura in the field. In several cases engrafted animals showed the remarkable ability to expel their parasite load. The model will thus be useful for analysing human immune responses to trichuriasis under highly controlled laboratory conditions impossible to achieve in the field.

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