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PubMed1998

Effects of immunotherapy on experimental immunodeficiency-related lymphoproliferative disease.

BACKGROUND: Human lymphokine-activated cells (LAK cells) and interferon alpha (IFN-alpha) have been used clinically in the therapy of posttransplant lymphoproliferative disease (PTLD). However, the efficacy of such therapy has not been extensively tested under controlled experimental conditions. METHODS: A B-cell line, derived from PTLD tissue and clonally related to the parent lesion, was tested for its response to IFN-alpha in vitro. The effects of LAK cells and IFN-alpha therapy were examined in a severe combined immunodeficiency disease (SCID) mouse model in vivo. RESULTS: The PTLD cell line studied showed a 30% decrease in the rate of growth upon incubation with 500 U/ml of IFN-alpha. This in vitro response was also reproduced in vivo, in tumor therapy studies conducted in SCID mice. The magnitude of this inhibitory effect in vivo was a function of tumor burden and dose of IFN-alpha. In parallel experiments, LAK cells reduced the tumorigenicity of a lymphoblastoid cell line derived from the peripheral blood of a patient with PTLD, and prolonged the survival of SCID-beige mice with established lymphoproliferative disease. In contrast with two prior studies, in which the use of autologous cytotoxic T cells was found to be necessary, we found the administration of third-party non-HLA-matched LAK cells also to be effective in reducing tumor burden. CONCLUSIONS: These observations demonstrate the efficacy of immunotherapy for lymphoproliferative disease under controlled experimental conditions, and validate currently ongoing efforts exploring the utility of such therapy in the clinical setting.

Animals↗

PubMed1997

Neutrophils play a critical role in early resistance to amebic liver abscesses in severe combined immunodeficient mice.

Animal models of liver abscess formation with Entamoeba histolytica suggest that the neutrophil is the first cell of the host immune system to interact with the invading ameba. In vitro studies have suggested that lysis of neutrophils by virulent amebae may exacerbate the damage seen in amebic liver abscesses. To investigate the role of neutrophils in vivo, we used the severe combined immunodeficient (SCID) mouse model of amebic liver abscess formation and compared liver damage in neutrophil-depleted and control mice. We found that neutrophil-depleted animals have significantly larger amebic liver abscesses at early stages of infection and that abscesses in neutrophil-depleted SCID mice lack the prominent inflammatory cell ring seen in amebic liver abscesses in control SCID mice. These data suggest that neutrophils play a protective role in the early host response to amebic infection of the liver.

Animals↗

PubMed2005

Inhibition of Ki-67 in a renal cell carcinoma severe combined immunodeficiency disease mouse model is associated with induction of apoptosis and tumour growth inhibition.

OBJECTIVE: To evaluate the effects of suppressing the expression of Ki-67 (expressed in proliferating cells) by antisense oligonucleotides (asON) directed against Ki-67 (which specifically inhibit the proliferation of tumour cells and tumour growth in cell culture and in subcutaneous murine tumour models) on the growth, cell viability and angiogenic activity of a preclinical renal cell carcinoma (RCC) severe combined immunodeficiency disease (SCID) mouse model. MATERIALS AND METHODS: Human RCC cells (SK-RC-35) were incubated with asON and control ON in the presence of a cationic lipid in monolayer cell culture. To test Ki-67 as a target for antitumour therapy in more complex models, asON were administered to three-dimensional RCC (SK-RC-35) spheroid cultures and to SCID mice bearing subcutaneous SK-RC-35 xenografts. For animal studies, 1 x 10(6) SK-RC-35 cells were implanted subcutaneously. Subsequently, asON or ON were injected intraperitoneally daily for 14 days at 10 mg/kg/day. Tumour size, weight and status of metastasis were documented daily and after death, respectively. The number of apoptotic cells, Ki-67-positive cells and the microvessel density in tumour sections was determined immunohistochemically. Quantitative reverse transcription-polymerase chain reaction of Ki-67 mRNA was also assessed for the tumours. RESULTS: Treatment of RCC cells with asON resulted in a specific inhibition of cell growth in monolayer and spheroid cell culture. Systemic administration of Ki-67-directed asON significantly decreased tumour growth (P = 0.009) in SCID mice. Immunohistochemical staining of tumour specimens showed stronger inhibition of Ki-67-positive cells in asON-treated tumours (mean 27.8%) than in controls (mean 42.5-57%). Furthermore, there were about twice as many apoptotic cells after asON treatment. There was no significant difference among treatment groups for microvessel density. CONCLUSION: These results indicate that Ki-67 represents a suitable antiproliferative target, and that asON are a potent agent inhibiting tumour growth and apoptosis, but not tumour vascularization, in human RCC.

Animals↗

PubMed1999

New concepts for the development of autoimmune exocrinopathy derived from studies with the NOD mouse model.

The non-obese diabetic (NOD) mouse is now recognized as an appropriate model to study autoimmune exocrinopathy prevalent in human Sjögren's syndrome patients. With increasing age, NOD mice undergo histopathological changes similar to human Sjögren's syndrome patients, but more importantly, exhibit the same clinical manifestation of declining exocrine tissue secretory function. Studies with the immunodeficient NOD-scid mouse have provided evidence for the temporal loss in the expression of several major salivary proteins and a decreased presence of acinar cells in salivary tissues. The diminished presence of acinar cells is accompanied by an increase in the enzymes associated with apoptosis in the absence of T- and B-lymphocytes. Despite these alterations, NOD-scid mice, unlike NOD mice, do not lose secretory function. Recent analyses of a second congenic NOD strain, the NOD.Igmnull, which lacks B-lymphocytes, indicate the histological presence of a T-cell infiltrate of the exocrine glands, increased caspace activity and induction of the biochemical alterations in protein expression observed in NOD and NOD-scid mice. NOD.Igmnull mice also do not lose secretory function, but can be manipulated to generate a reduced secretory response following the infusion of IgG fractions from autoimmune NOD mice or Sjögren's syndrome patients. These observations, in the absence of components of the adaptive arm of the immune system, have given rise to the concept that autoimmune exocrinopathy develops in two phases. The initial phase is lymphocyte independent and occurs as a consequence of an innate error in exocrine tissue homeostasis or differentiated function. The subsequent tissue specific immunological attack, generated in part by B-cell autoantibodies, is responsible for the loss of secretory function. Our preliminary observations in both NOD mice and Sjögren's syndrome patients is that antibody directed against the cell surface muscarinic/cholinergic receptors appears to play an important part in the onset of clinical disease.

Animals↗

PubMed1995

An anti-CD72 immunotoxin against therapy-refractory B-lineage acute lymphoblastic leukemia.

CD72 is a broadly expressed B-lineage specific surface antigen. We used J3-109(anti-CD72) monoclonal antibody to examine primary neoplastic cells from patients with acute leukemia for CD72 expression. CD72 was present at high levels in 70 of 100 B-lineage acute lymphoblastic leukemias (ALL), but it was not expressed on cells from 23 T-lineage ALL patients or 9 acute myeloblastic leukemia patients. We have prepared an anti-CD72 immunotoxin by conjugating J3-109 monoclonal antibody to the ribosome-inactivating protein, PAP.J3-109-PAP effectively killed > 99.9% of clonogenic blasts from a CD72+ B-lineage ALL cell line. We used a SCID mouse model of aggressive human pre-B ALL to evaluate the in vivo anti-leukemic efficacy of the J3-109-PAP immunotoxin. An intravenous challenge with 1 x 10(6) NALM-6-UM-1(pre-B ALL) cells caused 100% of SCID mice to die of disseminated leukemia within 41 days. Importantly, a three-day treatment with non-toxic doses of J3-109-PAP significantly improved event-free survival of SCID mice. The Kaplan-Meier estimate (+/- standard error) of the probability of event-free survival at 2 months after inoculation of NALM-6-UM-1 cells was 40 +/- 16% for SCID mice treated with a total of 15 micrograms J3-109-PAP (median survival = 58 days) as compared to 0 +/- 0% for PBS treated mice (median survival = 34 days). At 6 months after the inoculation of NALM-6-UM-1 cells, 10 +/- 9% of the J3-109-PAP treated SCID mice were still alive with no evidence of leukemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

In vitro and in vivo anti-leukemic efficacy of cyclic AMP modulating agents against human leukemic B-cell precursors.

We show that the adenylate cyclase activating diterpine, forskolin, the phosphodiesterase inhibitor, aminophylline, and the permeant cAMP analog dibutyryl cAMP inhibit the in vitro clonogenic growth of leukemic B-cell precursors. We also used a SCID mouse xenograft model of refractory human B-cell precursor leukemia to evaluate the anti-leukemic effect of aminophylline in vivo. Treatment with aminophylline (6 mg/kg bolus followed by 0.1-0.5 mg/kg/hour x 7 days) significantly prolonged the event-free survival of SCID mice (median survival of control mice, 39 days, N = 79; median survival of aminophylline-treated mice, 60 days, N = 10; P < 0.0001 by log-rank test) and it was more effective than treatment with vincristine (median survival = 51 days, N = 5) or L asparaginase (median survival = 44 days, N = 5). However, aminophylline was not as effective as methylprednisolone (median survival: 103 days, N = 5). These results indicate that cAMP modulating agents may be useful in treatment of refractory human B-cell precursor leukemia.

Aminophylline↗

PubMed1993

The in vitro action of FK 565, bleomycin and cyclosporin A on different cell populations, with respect to the release of GM-CSF in the mouse.

The experimental immunostimulatory tripeptide FK 565, the anti-tumor antibiotic Bleomycin and the immunosuppressive agent Cyclosporin A were examined for their in vitro effects on granulocyte-macrophage colony stimulating factor (GM-CSF) production utilizing different cell populations from three distinct murine stains. FK 565 produced an increase in GM-CSF release in all three experimental models used, providing evidence that FK 565 is among other things, a macrophage stimulating agent. Bleomycin increased GM-CSF release in the BALB/c and the 'Scid' mouse. Paradoxically with cells from the 'nude' mouse a significant decrease was observed, indicating that Bleomycin may induce a suppressive effect on B-cells. Cyclosporin A was found to inhibit the release of GM-CSF from BALB/c mice, however, no effect was observed in either 'nude' or 'Scid' mice.

Adjuvants, Immunologic↗

PubMed1997

Differential maintenance of primitive human SCID-repopulating cells, clonogenic progenitors, and long-term culture-initiating cells after incubation on human bone marrow stromal cells.

Many experimental and clinical protocols are being developed that involve ex vivo culture of human hematopoietic cells on stroma or in the presence of cytokines. However, the effect of these manipulations on primitive hematopoietic cells is not known. Our severe combined immune-deficient mouse (SCID)-repopulating cell (SRC) assay detects primitive human hematopoietic cells based on their ability to repopulate the bone marrow (BM) of immune-deficient non-obese diabetic/SCID (NOD/SCID) mice. We have examined here the maintenance of SRC, colony-forming cells (CFC), and long-term culture-initiating cells (LTC-IC) during coculture of adult human BM or umbilical cord blood (CB) cells with allogeneic human stroma. Transplantation of cultured cells in equivalent doses as fresh cells resulted in lower levels of human cell engraftment after 1 and 2 weeks of culture for BM and CB, respectively. Similar results were obtained using CD34+-enriched CB cells. By limiting dilution analysis, the frequency of SRC in BM declined sixfold after 1 week of culture. In contrast to the loss of SRC as measured by reduced repopulating capacity, the transplanted inocula of cultured cells frequently contained equal or higher numbers of CFC and LTC-IC compared with the inocula of fresh cells. The differential maintenance of CFC/LTC-IC and SRC suggests that SRC are biologically distinct from the majority of these in vitro progenitors. This report demonstrates the importance of the SRC assay in the development of ex vivo conditions that will allow maintenance of primitive human hematopoietic cells with repopulating capacity.

ADP-ribosyl Cyclase↗

PubMed2000

Cutting edge: IL-15 costimulates the generalized Shwartzman reaction and innate immune IFN-gamma production in vivo.

Sequential administration of LPS to SCID mice results in the generalized Shwartzman reaction, manifesting as rapid mortality via cytokine-induced shock. Here we demonstrate that in vivo neutralization of IL-15 before LPS priming significantly reduced lethality in this reaction (p = 0.0172). We hypothesize that LPS priming induces IL-12 and IL-15 that costimulate NK cell-derived IFN-gamma. Such IFN-gamma may then in turn sensitize macrophages to elicit the Shwartzman reaction following a subsequent LPS challenge. Supporting this, IL-12 and IL-15 synergized to induce murine NK cell IFN-gamma production in vitro. LPS stimulation of SCID mouse splenocytes resulted in measurable IFN-gamma production, which was reduced when IL-15 was neutralized or IL-2/15Rbeta was blocked. Pretreatment with either anti-IL-2/15Rbeta or anti-IL-15 Abs reduced serum IFN-gamma protein following LPS administration to SCID mice. Collectively, these data provide the first in vivo evidence that IL-15 participates in LPS-induced innate immune IFN-gamma production and significantly contributes to the lethal Shwartzman reaction.

Animals↗

PubMed1997

Comparison of the potency and therapeutic efficacy of the anti-CD7 immunotoxin HB2-saporin constructed with one or two saporin moieties per immunotoxin molecule.

Immunotoxins that carry two toxin molecules to the target cell should in theory have a greater anti-tumour effect than those that carry just one. We have investigated the therapeutic efficacy of two anti-CD7-saporin immunotoxins constructed with one saporin (HB2-Sap 1-mer) or two saporin molecules (HB2-Sap 2-mer) per immunotoxin molecule. In vitro, the 2-mer immunotoxin was 5.6 times more effective than the 1-mer immunotoxin at inhibiting protein synthesis in the CD7+ human T-cell acute lymphoblastic leukaemia (T-ALL) cell line HSB-2 and was also more effective at inhibiting HSB-2 cell proliferation. Flow cytometry revealed that the 2-mer immunotoxin had a reduced binding capacity to HSB-2 cells compared with the 1-mer immunotoxin or native HB2 antibody. In therapy studies in SCID mice with disseminated HSB-2 human leukaemia, the 2-mer immunotoxin performed marginally better than the 1-mer immunotoxin, but log-rank analysis did not reveal any significant differences between the two therapy groups. We therefore conclude that, although the 2-mer immunotoxin performed better than the 1-mer immunotoxin against target HSB-2 cells in vitro, this improved performance was not reflected as an improved in vivo therapeutic outcome in the SCID mouse model.

Animals↗

PubMed2004

Human skin preserved in anhydric sodium chloride for months can be successfully transplanted.

Human skin can be preserved in pulverized sodium chloride dehydrated at 240C for 2 hours at room temperature for periods of weeks or months and successfully transplanted to scid mouse, retaining its normal morphological structure. Fragment of skin of a size of 10 x 10 x 6 mm were harvested during elective vascular and orthopaedic surgery of lower limbs, dried of blood and placed in anhydric sodium chloride powder in tight sealed containers. Prior to transplantation to scid mice, the specimens were desalinated and rehydrated. Specimes preserved for 1 to 6 months and harvested 3-4 weeks after transplantation revealed intensive incorporation of bromdeoxyuridine (BrdU) into basal keratinocytes. They expressed p63 and CD29 (stem cells, and transient cells antigens), PCNA (proliferating cell nuclear antigen) and cytokeratin 16 specific for proliferating keratinocytes. Dermal fibroblasts and few large HLA II cells showed a normal structure. Bacterial flora of skin did not change after grafting. We conclude that human skin can survive in a dehydrated state in sodium chloride for months and after transplantation the epidermal basal layer cells give rise to keratinocyte progenies. Skin fibroblasts and some resident immune cells can also survive.

Anhydrides↗

PubMed2002

The hepatitis C virus (HCV)-Trimera mouse: a model for evaluation of agents against HCV.

The lack of small-animal models that are suitable for evaluation of agents used to treat infection with hepatitis C virus (HCV) severely hinders the assessment of potential new therapies for the disease. This study created such a model, termed the "HCV-Trimera" model. The HCV-Trimera model was developed by using lethally irradiated mice, reconstituted with SCID mouse bone marrow cells, in which human liver fragments infected ex vivo with HCV had been transplanted. Viremia (positive-strand HCV RNA levels) in HCV-Trimera mice peaked at approximately day 18 after liver transplantation, and an infection rate of 85% was reached. Viral replication in liver grafts was evidenced by the presence of specific negative-strand HCV RNA. The usefulness of this model for evaluation of anti-HCV agents was demonstrated by the ability of a small molecule (an HCV internal ribosomal entry site inhibitor) and an anti-HCV human monoclonal antibody (HCV AB(XTL)68) to reduce virus loads in HCV-Trimera mice in a dose-dependent manner.

Animals↗

PubMed2005

HPA binding and metastasis formation of human breast cancer cell lines transplanted into severe combined immunodeficient (scid) mice.

Six human breast cancer cell lines were injected subcutaneously into scid mice and their in vivo growth behaviour and HPA binding pattern were analysed. Furthermore, the role of HPA binding glycoconjugates concerning the adhesion to endothelial cells in vitro was investigated. Four of the tested cell lines engrafted in the scid mouse model but they showed considerable variations concerning their growth behaviour, their metastatic potential and their HPA binding pattern. HPA inhibited adhesive interactions between cell lines derived from metatstatic sources and tumour necrosis factor (TNF)alpha stimulated endothelial cells. The transplantation of HPA defined breast cancer cell lines into scid mice is a useful animal model for the research of breast cancer and its metastasis. The HPA binding glycoconjugates appear to be associated with adhesive interactions between metastasising tumour cells and endothelial cells.

Acetylgalactosamine↗

PubMed1999

The ability of p53 to activate downstream genes p21(WAF1/cip1) and MDM2, and cell cycle arrest following DNA damage is delayed and attenuated in scid cells deficient in the DNA-dependent protein kinase.

scid mouse embryonic fibroblasts are deficient in DNA-dependent protein kinase activity due to a mutation in the C-terminal domain of the catalytic subunit (DNA-PKcs). When exposed to ionizing radiation, the increase in levels of p53 was the same as in normal mouse embryonic fibroblasts. However, the rise in p21(WAF1/cip1) and mdm2 was found to be delayed and attenuated, which correlated in time with delayed onset of G1/S arrest by flow cytometric analysis. The p53-dependent G1 checkpoint was not eliminated: inactivation of p53 by the E6 protein in scid cells resulted in the complete loss of detectable G1/S arrest after DNA damage. Immunofluorescence analysis of normal cells revealed p53 to be localized predominantly within the cytoplasm prior to irradiation and then translocate to the nucleus after irradiation. In contrast, scid cells show abnormal accumulation of p53 in the nucleus independent of irradiation, which was confirmed by immunoblot analysis of nuclear lysates. Taken together, these data suggest that loss of DNA-PK activity appears to attenuate the kinetics of p53 to activate downstream genes, implying that DNA-PK plays a role in post-translational modification of p53, without affecting the increase in levels of p53 in response to DNA damage.

Animals↗

PubMed1999

Human Taenia in severe combined immunodeficiency (SCID) mice.

A rodent model for the development of the larval stages of human taeniid tapeworms would help advance immunodiagnosis in human and domestic animals and vaccine development for cysticercosis cellulosae or bovis in domestic animals. Here, Akira Ito and Mamoru Ito review recent results demonstrating the potential of the severe combined immunodeficiency (SCID) mouse for supporting development of the larval stages of Taenia saginata asiatica, T. saginata and T. solium.

Animals↗

PubMed1994

Therapy of human T-cell acute lymphoblastic leukaemia in severe combined immunodeficient mice with two different anti-CD7-saporin immunotoxins containing hindered or non-hindered disulphide cross-linkers.

A SCID mouse model of human T-ALL has been used to determine the in vivo therapeutic efficacy of two anti-CD7-saporin immunotoxins constructed with either a hindered (HB2-SMPT-Sap) or non-hindered (HB2-SPDP-Sap) disulphide bond between antibody and saporin. Groups of 10 SCID mice were injected intravenously (i.v.) with 2 x 10(6) human T-ALL HSB-2 cells followed seven days later by i.v. injection with either a single dose or with 3 doses of HB2-SPDP-Sap or HB2-SMPT-Sap given on alternate days. Control groups received equivalent sham injections of PBS or molar equivalent amounts of unconjugated HB2 antibody+saporin. Animals receiving a single dose of HB2-SMPT-Sap showed better survival than animals receiving a single dose of HB2-SPDP-Sap but the difference was not shown to be significant by log-rank analysis. When given as a triple dose both immunotoxins performed similarly. Comparison of single-dose with triple-dose IT therapy revealed that the therapeutic effect of a triple dose of HB2-SPDP-Sap was significantly better than that of single dose, but this was not the case with HB2-SMPT-Sap. Pharmacokinetic studies of HB2-SPDP-Sap and HB2-SMPT-Sap in normal and HSB-2 leukaemia bearing SCID mice failed to reveal any difference in clearance rates for these two IT's. We conclude from these studies that there is no therapeutic advantage to be gained from constructing the HB2-Sap IT with a hindered disulphide bond in this particular model of human T-ALL.

Animals↗

PubMed1999

Myoblast transplantations lead to the expression of the laminin alpha 2 chain in normal and dystrophic (dy/dy) mouse muscles.

Laminin-2 is part of the basement membrane of the skeletal muscle fibers. The laminin alpha 2 chain is absent or drastically reduced in a subgroup of congenital muscular dystrophy patients, and in the severely affected dystrophic dy/dy mouse. We previously reported that heterogeneous primary mouse muscle cell cultures conferred laminin alpha 2 chain expression in dy/dy mice muscles upon cell transplantation. In the present study we investigated whether pure myoblast cell lines were able to confer laminin alpha 2 chain expression in vivo. We observed that: (1) xeno-transplantation of non-immortalized human myoblast in SCID mouse muscles allows human laminin alpha 2 chain expression; (2) allotransplantation of the permanent G8 mouse myoblast cell line in dy/dy muscles allows the expression of the murine laminin alpha 2 chain; and (3) allo-transplantation of the D7 dystrophic dy/dy cell line allows the formation of new and hybrid muscle fibers in dy/dy muscle in the absence of laminin alpha 2 chain expression. We conclude that normal myoblasts are able to restore the expression of an extracellular skeletal muscle protein and that the absence of laminin-2 does not prevent transplanted muscle cells from participating in the formation of myofibers. Myoblasts are, therefore, attractive tools for further exploration of gene complementation strategies in the animal models of congenital muscular dystrophy.

Animals↗

PubMed1989

Bone marrow cells from young and old New Zealand black mice can reconstitute B lymphocytes in severe combined immunodeficient recipients.

The formation of B lymphocytes in young New Zealand Black (NZB) mice proceeds at an accelerated rate, resulting in a deficiency of B lineage progenitors in mice of 15 weeks of age and older. Multiple studies have indicated that intrinsic defects in B lineage cells as well as in the hemopoietic microenvironment in which they develop contribute to these cellular abnormalities. To determine whether the B-cell hyperactivity observed in young mice could be observed in a normal environment, bone marrow cells from young (4 weeks or less) NZB donors were transplanted into Severe Combined Immunodeficient (SCID) mice that have a marked deficiency of lymphocytes but an apparently normal hemopoietic microenvironment. Engraftment of donor lymphoid cells can occur without pretransplant conditioning regimens, thus minimizing the chances of transferring microenvironmental elements. Marrow from young NZB donors reconstituted surface IgM-expressing B cells and CFU-B (B-cell colony-forming unit) in the marrow of SCID mouse recipients to levels comparable to that observed with donor NZB.xid marrow. The latter mice carry the xid gene that ameliorates the defects exhibited by B lineage cells of NZB mice. Both the number of surface IgM-expressing B cells and CFU-B were higher in the spleen of SCID mice that received NZB grafts than marrow cells from donor BALB/c or NZB.xid mice. Marrow from young NZB donors also reconstituted Thy-1, L3T4 and Lyt2-expressing cells in the spleen to levels higher than observed with young NZB.xid donor cells. The transplantation of marrow from 6-month-old NZB donors made it possible to test whether B lineage cells were present in that tissue and could mediate reconstitution in the normal SCID environment. Marrow from old NZB donors did reconstitute B cells in the marrow and spleen of SCID recipients. The level of reconstitution was comparable to that mediated by young BALB/c cells and twice that of old NZB.xid donor cells. The absolute number of splenic CFU-B was also higher in recipients of old NZB marrow as compared to young BALB/c cells. Old NZB.xid donor marrow reconstituted splenic Thy-1, L3T4 and Lyt2 T cells to levels less than observed with NZB donor cells. Analysis of serum Ig in recipients of old NZB cells indicated higher levels of total IgM as compared to mice engrafted with NZB.xid cells, and anti-single stranded DNA antibodies were detected.

Age Factors↗