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At least 199 records · Page 11Linked to original sources
PubMed1991

SCID mouse model of Epstein-Barr virus-induced lymphomagenesis of immunodeficient humans.

Immunodeficient humans are at very high risk of developing Epstein-Barr virus (EBV)-induced lymphomagenesis. Severe combined immunodeficient mice (SCID) have been shown to develop lymphoproliferative disease (LPD) following transfer of peripheral blood leukocytes (PBL) with latent EBV. To study mechanisms of lymphomagenesis, we compared results of engraftment of PBL from normal donors and immunodeficient donors with X-linked lymphoproliferative disease (XLP). Graft-versus-host disease (GVHD) developed in 6 of 10 SCID mice 4 to 8 weeks following transfer of PBL from normal donors. In contrast, none of 9 mice engrafted with PBL from XLP patients with T-cell defects showed GVHD. LPD developed in mice regardless of the immune competence of the donors. The expression of EBV-encoded proteins, results of immunophenotyping, and karyotyping of the LPD lesions revealed lethal oligoclonal LPD owing to transfer of latent EBV in B cells in mice engrafted with PBL from seropositive donors. Polyclonal LDP developed in mice engrafted with PBL from seronegative patients which were infected with B95-8 virus 6 weeks after transfer of the cells. This model is useful for investigating mechanisms of EBV-induced LDP in immunodeficient patients.

Animals↗
PubMed1995

Evaluation of a two-phase scid mouse model preconditioned with anti-interferon-gamma monoclonal antibody for drug testing against Cryptosporidium parvum.

One 1-mg injection of anti-interferon-gamma monoclonal antibody (anti-IFN-gamma MAb) into newly weaned scid mice 2 h before challenge with Cryptosporidium parvum oocysts markedly exacerbated the course of the infection for > or = 47 days, compared with challenged mice that received an equivalent dose of irrelevant MAb. Oocyst excretion in feces started 4-6 days after challenge and continued at high levels for > or = 47 days. Loss of body weight was also apparent. The extent and distribution of mucosal infection were profound, involving the stomach and several segments of the small and large intestines. The acute phase, which involved infection of the gut, was during the first 25 days after challenge. The following chronic phase consistently involved, in addition, infection of the hepatobiliary tract. The acute phase is a useful model in which to test luminally active drugs, while the chronic phase may be used in the future to test drugs that are active against hepatobiliary tract infections as well.

Amebicides↗
PubMed1996

Transfusion of polarized TH2-like cell populations into SCID mouse cardiac allograft recipients results in acute allograft rejection.

It has been hypothesized that TH1 cells mediate the archetypical cell-mediated immune response of acute allograft rejection, whereas TH2 cells promote allograft acceptance. To test this, we transfused SCID cardiac allograft recipients with polarized TH1-like or TH2-like graft-reactive T cells, and monitored graft function and graft-reactive immune responses in the graft recipients. Polarized THl-like cells, which were generated in vitro by stimulating syngeneic splenocytes with donor alloantigens in the presence of anti-IL-4 mAb, produced IFNg but not IL-4 when restimulated with donor alloantigen. Polarized TH2-like populations, which are generated in vitro by stimulating syngeneic splenocytes with donor alloantigens in the presence of IL-4, produced IL-4 but not IFNg when restimulated with donor alloantigen. Interestingly, bioassays of culture SN from restimulated TH1 but not TH2 cells revealed IL-2 production, although LDA analyses revealed that the TH1 and TH2 cells had identical frequencies of IL-2-producing cells. Transfusion of THl-like cells into SCID cardiac allograft recipients resulted in acute rejection within 7-10 days that was characterized by cellular infiltration, myocyte necrosis, and edema. Graft-infiltrating cells (GIC) recovered from TH1-transfused animals contained large numbers of graft-reactive IL-2-producing cells (68-269/10(6) GIC), but no LDA-detectable IL-4-producing cells. These data support the hypothesis that donor-reactive TH1 cells can promote acute allograft rejection. In contrast to the hypothesis, transfusion of the polarized TH2-like population into SCID cardiac allograft recipients also resulted in histologically similar acute rejection within 7-10 days. Infiltrating cells recovered from TH1-transfused allografts contained large numbers of graft-reactive (109-1458/10(6) GIC), LDA-detectable, IL-4-producing cells--indicating that the TH2 cells had arrived at the graft-but promoted acute allograft rejection rather than allograft acceptance.

Acute Disease↗
PubMed1995

Limitations of the severe combined immunodeficiency (SCID) mouse model for study of human B-cell responses.

Mice lacking functional T and B lymphocytes offer an in vivo animal model for the study of human immune functions. We have attempted to optimize the reconstitution of severe combined immunodeficiency (SCID) mice with human peripheral blood lymphocytes (PBL) using radiation, anti-asialo GM1 antibody or cyclophosphamide (Cy) treatment of the mice and in vitro stimulation of human PBL with interleukin (IL)-2 prior to their transfer to the mice. Total human IgG and tetanus-toxoid (TT)-specific human IgG responses of the mice were used as parameters of successful reconstitution. Treatment of the mice with anti-asialo GM1 antibody significantly enhanced total human IgG levels, but not TT-specific antibody responses, whereas irradiation or Cy treatment of the mice had no effect on human antibody production. In vitro treatment of human PBL with IL-2 prior to engraftment significantly decreased total human IgG responses of human PBL-grafted SCID mice. The immune responses of individual mice within a group were highly variable, which constitutes a major disadvantage of this model.

Animals↗
PubMed1999

Preliminary experience with subcutaneous human ovarian cortex transplantation in the NOD-SCID mouse.

Xenogeneic transplantation of ovarian cortex into an immunodeficient animal host may be an approach toward fertility preservation for young female patients undergoing cancer therapy. Our objective was to evaluate the development of follicles in human ovarian cortex placed s.c. in non-obese diabetic-severe combined immune deficiency (NOD-SCID) mice (n = 54). The following variables were compared: 1) male versus female mice as hosts, 2) intact versus pituitary down-regulated mice, and 3) warm versus cold tissue transport. After 2 wk, 37 of 50 (74%) of the human xenografts contained follicles. At 12 wk after transplantation, exogenous gonadotropin stimulation resulted in follicle growth in 19 of 37 (51%) of the grafts, including the development of antral follicles, which could be palpated and visualized through the mouse skin. Significantly more developing follicles were identified in male versus female mice (13 of 17 vs. 6 of 20, respectively; p = 0.013) after stimulation. No difference was found between intact and pituitary down-regulated mice as hosts. Follicular survival was significantly increased by warm versus cold tissue transport. Our results suggest that s.c. ovarian cortex xenografting into NOD-SCID mice is feasible. Primordial follicles in ovarian xenografts retain their developmental potential and form antral follicles following gonadotropin stimulation.

Animals↗
PubMed2003

Effect of laparotomy and CO(2) pneumoperitoneum on tumor growth of human colon carcinoma and expression pattern of tumor-associated proteins in the SCID mouse.

BACKGROUND AND AIMS: The impact of laparoscopy on tumor progression is still unclear. This study investigated the effect of CO(2) pneumoperitoneum on the intra-abdominal growth of human colon carcinoma independently of the effect of the immune system. METHODS: SCID mice underwent either median laparotomy or laparoscopy. Human colon carcinoma cells were implanted into the upper abdomen. The control group was not operated on following cell injection. Tumor growth and the protein expression pattern of proliferation marker Ki67, cell-cell adhesion molecules E-cadherin, alpha- and beta-catenin, and cell-extracellular matrix adhesion molecules CD44 v5 and v6 in tumor tissue were analyzed on postoperative day 14. RESULTS: Total tumor volume in the laparoscopy group significantly exceeded that in the laparotomy group. Immunohistochemistry revealed reduced expression of alpha-catenin and elevated expression on beta-catenin and CD44 v5 in the tumor tissue of the laparoscopy group. CONCLUSION: The expression pattern of proteins associated with tumor progression and the increase in tumor growth suggest an increased risk of laparoscopy at least for the growth of advanced human colon carcinoma.

Animals↗
PubMed2005

Tetrahydrocannabinol suppresses immune function and enhances HIV replication in the huPBL-SCID mouse.

Epidemiologic studies identify marijuana as a potential cofactor in the development and progression of HIV infection. To evaluate this interaction we employed a hybrid model in which human peripheral blood leukocytes (PBL) were implanted into severe combined immunodeficient mice (huPBL-SCID) and infected with an HIV reporter construct in the presence or absence of tetrahydrocannabinol (THC) exposure. Administration of THC alone, in the absence of HIV, decreased CD4 counts and the CD4:CD8 ratio. Co-administration of THC and HIV did not reduce CD4 counts further, but significantly increased the percentage of HIV-infected PBL when compared to saline-treated animals (17+/-4.6% vs. 7+/-1.4%). Quantitative PCR confirmed a 50-fold increase in systemic viral load in THC-treated animals. The CCR5 and CXCR4 chemokine receptors function as coreceptors essential for HIV infection. Administration of THC for 5 days increased the percentage of PBL expressing CCR5 and, to a lesser extent, CXCR4. This effect was lost after 10 days of THC administration, but the number of HIV-infected cells had significantly increased by that time suggesting a role for early upregulation of these coreceptors in the pathogenic effect of THC. Finally, the impact of treatment on the number of human interferon-gamma (IFN-gamma) producing cells was determined by ELISPOT. Both THC and HIV infection independently decreased the number of IFN-gamma producing cells and co-administration produced additive effects. These results suggest that exposure to THC in vivo can suppress immune function, increase HIV coreceptor expression, and act as a cofactor to significantly enhance HIV replication.

Animals↗