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At least 163 records · Page 9Linked to original sources
PubMed1986

The use of plasmapheresis, lymphocytapheresis, and staph protein-A immunoadsorption as an immunomodulatory therapy in patients with AIDS and AIDS-related conditions.

Circulating immune complexes, autoantibodies, and suppressor factors to normal lymphoproliferation may play an important role in the induction and maintenance of the cellular immunodeficiency characteristic for the acquired immunodeficiency syndrome (AIDS) and its related conditions. In order to explore the possibility that the removal of circulating humoral factors may have an immunomodulatory effect in patients with AIDS and AIDS-related conditions (ARC), we used apheresis procedures to treat patients with different clinical presentations of AIDS and ARC. Five patients with AIDS and opportunistic infections were treated with plasmapheresis. Four patients with AIDS and Kaposi's sarcoma without opportunistic infections were treated with staph protein-A immunoadsorption and two patients with ARC and peripheral neuropathy were treated with lymphoplasmapheresis. The treatments were tolerated well by all patients. Effective removal of circulating humoral immune factors was observed in all three groups. No significant clinical benefit was seen in the patients with AIDS and opportunistic infections treated with plasmapheresis. Partial tumor responses were observed in three of the four patients with AIDS related Kaposi's sarcoma treated with staph protein-A plasma perfusion, and resolution of neurologic symptoms was seen in both patients with ARC and peripheral neuropathy treated with lymphoplasmapheresis. Our preliminary results suggest that lymphoplasmapheresis may be an effective treatment modality for patients with ARC related peripheral neuropathy, that protein-A immunoadsorption is well tolerated by patients with AIDS-related Kaposi's sarcoma, and that this treatment has antitumor and immunomodulatory effects in these patients.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Lymphoproliferative disease in SCID mice reconstituted with human Sjögren's syndrome lymphocytes.

Patients with Sjögren's syndrome (SS) have increased frequency of non-Hodgkin's B-cell lymphoma. These lymphomas frequently use a specific subclass of kappa light chain (encoded by variable region gene segment Hum KV325) and exhibit bcl-2 protooncogene translocation t(14;18). In order to determine whether expansion of this B-cell subset could be reproduced in an animal model, immunodeficient SCID (CB-17) mice were reconstituted with lymphocytes from 4 different SS patients at high risk of the development of lymphoma. Tumor-like nodules developed in all 11 SCID mice that received at least 5 x 10(5) lymphocytes from SS salivary glands or peripheral blood samples. However, the tumor-like nodules in the SCID mice differed from SS lymphomas in vivo in that they (1) exhibited multiple immunoglobulin gene rearrangements; (2) did not have expansion of B-cells expressing the Hum KV325 K-light chain; and (3) lacked detectable t(14;18) translocations. Characterization of the SCID tumor-like nodules revealed a high level of Epstein-Barr virus (EBV) DNA, EBV-associated antigens (EA-R, EBNA-2, AND LMP), and the EBV-encoded cytokine BCRF-1 that is structurally similar to IL-10. These results demonstrate that the lymphoproliferation occurring in the salivary glands of SS patients is not reproduced in the SCID/hu chimeric mouse. It is likely that specific factors in the human salivary gland are required for development of lymphoma in SS patients and that such factors are not present in the SCID/hu chimeric mouse. Furthermore, EBV-induced lymphoproliferation, as seen in the SCID/hu chimera, does not lead to expansion of the same lymphoid subsets that occurs in vivo.

Animals↗
PubMed1995

Recombinant human IL-7 administration in mice affects colony-forming units-spleen and lymphoid precursor cell localization and accelerates engraftment of bone marrow transplants.

Murine reconstitution assays were used to investigate the effects of recombinant human interleukin-7 (rhIL-7) on myeloid and lymphoid precursors and on bone marrow engraftment. Reconstitution with bone marrow from rhIL-7-treated mice results in a 3.4-fold decrease in total colony-forming unit-spleen (CFU-S) activity (day 9) and an 18.1- and 11.9-fold decrease in its ability to generate thymocytes and splenic B lineage cells, respectively. In contrast, after reconstitution with splenocytes from rhIL-7-treated mice, CFU-S activity increased 23.6-fold (day 9) and the thymocyte and splenic B lineage cell regenerative capacity increased by 4.0- and 3.2-fold, respectively. In addition, CD43low+, B220low+ cells that contain pre-pro-B cells and pro-B cells were expanded two- to threefold and Ig mu-, B220+, CD2- and Ig mu-, B220+, CD2+ B lineage cells were expanded approximately 10-fold and 10- to 45-fold (depending on the tissue examined), respectively, after rhIL-7 treatment. Administration of rhIL-7 to irradiated mice transplanted with bone marrow resulted in accelerated T cell and B cell reconstitution by up to 2-4 weeks. Thus, rhIL-7 administration affects the distribution of myeloid and lymphoid precursors. Moreover, rhIL-7 administration accelerates murine bone marrow cell engraftment and therefore may be useful in reducing the engraftment time in bone marrow transplant patients.

Animals↗
PubMed1979

Immunotherapy of a murine sarcoma using specific antitumor immune RNA.

The effect of IRNA therapy in a polyoma-induced fibrosarcoma of C3H mice has been studied. Although a protocol that transferred in vitro cytotoxicity was used, no reduction in incidence of tumors, tumor size, or survival was demonstrated. In one experiment, enhancement of tumor growth occurred. It is concluded that cytotoxicity does not reflect in vivo changes and that therapeutic trials of IRNA are premature.

Animals↗
PubMed1981

In vivo evaluation of cell mediated immunity against human melanoma.

Evaluation of cell mediated immunity against human melanoma target cells was performed in an in vivo model using human tumor xenografts growing in Balb/c athymic mice. Intraperitoneal inoculation of 1 x 10(7) human melanoma cells produced carcinomatosis which lead to death of the animals at 23.8 +/- 2.6 days (N = 12). Peripheral blood lymphocytes (PBL) from normal donors were administered to tumor bearing mice, and survival times of 22.0 +/- 2.3 days were observed (N = 8). Peripheral blood lymphocytes from the four of five normal donors which had been presensitized on monolayers of melanoma tissue culture cells in vitro failed to prolong host survival times. In contrast, PBL obtained from 15 or 20 melanoma patients were found to prolong survival of the tumor bearing nude mice. Of these 15 patients, 8 were undergoing specific active immunotherapy, while 7 had not been sensitized except by the disease process. The ability of PBL obtained from patients to prolong survival of tumor bearing animals did not appear to correlate with either the stage of the disease or the patient's clinical course. The possible mechanisms for the prolonged survival and usefulness of this model are discussed.

Animals↗
PubMed2006

In vivo cellular imaging of lymphocyte trafficking by MRI: a tumor model approach to cell-based anticancer therapy.

The aim of this study was to demonstrate the feasibility of in vivo cell tracking to monitor anticancer cell therapy by means of a high-resolution noninvasive MRI method. Ovalbumin-specific splenocytes (OT-1) labeled with anionic gamma-Fe2O3 superparamagnetic iron oxide (SPIO) nanoparticles were adoptively transferred into C57BL/6 mice with growing ovalbumin-expressing tumors. OT-1 cells were tracked in vivo by 7 T MRI 24, 48, and 72 hr after they were injected. The results showed significant negative enhancement of the spleen at 24 hr, and of the tumor at 48 and 72 hr, after labeled cell injection. This suggests that the lymphocytes initially homed toward the spleen and were then recruited by the tumor. The presence of labeled cells was confirmed in ex vivo by 9.4 T microimaging of tumors and magnetic sorting of spleen cells. These results confirm that MR tracking of lymphocytes is feasible in vivo. This high-resolution imaging method could be used to improve the monitoring of immune cell therapy.

Animals↗
PubMed1986

The fetal liver as an alternative stem cell source for hemolymphopoietic reconstitution.

In mammalian ontogeny, the liver constitutes the primary hematopoietic organ for some time. Fetal liver cells (FLC) are rich in hematopoietic stem cells with a high proliferative potential but contain few post-thymic T cells. In animal studies, FLC restored hematopoiesis without severe graft-versus-host disease. However, genetic disparity between donor and host frequently limited durable engraftment and prevented or protracted complete immune reconstitution in most fully allogeneic recipients. Some children with severe combined immunodeficiency have been cured by FLC infusion, whereas favorable effects in aplastic anemia, acute leukemia, and inborn errors of metabolism have been limited and badly understood. Fetal liver transplantation in animals may serve as a model for the analysis and management of complications associated with the transfer of purified hematopoietic stem cell grafts and aid in the development of future therapeutic strategies requiring rapidly proliferating stem cell populations.

Anemia, Aplastic↗
PubMed1993

Regulation of human IgE response in hu-PBL-SCID mice.

The human IgE response was investigated in hu-PBL-SCID mice created by ip injection of human PBL into C.B.17 scid/scid (scid) mice. With 30-100 x 10(6) PBL/mouse, 80 to 90% of the animals responded with human IgE serum levels of 3-1000 ng/ml after 2 weeks. PBL from all donors analyzed (total number > 20) responded with IgE production. The half-lives of human IgE, IgM, and IgG in scid mice were determined to test the possibility of a passive transfer of the immunoglobulins in contrast to de novo synthesis. The values found were 88, 128, and 126 hr, respectively. In general, immunoglobulin production of all isotypes continuously increased over a period of 7-9 weeks after PBL injection, indicating de novo synthesis had taken place. The kinetics of the IgE response exhibited two phases: An initial burst of IgE production occurred between Days 12 and 22. This burst reached levels of 25-70 ng/ml IgE. After a rapid decline to about 50% of the peak value there was a sustained, slow, increase of IgE production for several weeks, excluding a passive transfer for IgE. About half of the donors lacked the initial burst of IgE production and only exhibited a slowly rising IgE production that is indistinguishable from the slow phase of the former donor population. The levels reached in this second phase of IgE production were 20-40 ng/ml after 6-7 weeks. This kinetics may reflect the presence of two different B cell populations, of which only one is present in all donors. The initial IgE burst was only partially dependent on the presence of human IL-4, reflected by a partial inhibition of this response by a neutralizing monoclonal anti-IL-4 antibody. The IgE response in scid mice seems to consist therefore of an IL-4-independent and an IL-4-dependent part, indicating the response to be partially driven by preswitched B cells. Injection of exogenous recombinant human IL-4 (rhIL-4) was not suitable due to the short half-life of rhIL-4 in scid mice of 12 min. Attempts to supply a constant source of rhIL-4 by injection of IL-4-producing Chinese hamster ovary cells failed because of toxic effects produced by these cells. The human IgE production in the scid mice was suppressed by interferon-alpha (BD) to 60-80% compared to that of untreated mice. The suppression was not isotype specific, however, because production of IgG and IgM was inhibited to similar extents.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Human recombinant IL-2 augments immunoglobulin and induces rheumatoid factor production by rheumatoid arthritis lymphocytes engrafted into severe combined immunodeficient mice.

Recombinant (r) human IL-2 was administered in vivo to improve homing and engraftment of rheumatoid arthritis (RA) patients' peripheral blood mononuclear cells (PBMC) into severe combined immunodeficient (SCID) mice. Human rIL-2 treatment resulted in augmented human Ig production and induced IgM rheumatoid factor (RF) of human origin in SCID-RA chimeras. The increment of human serum IgG in SCID-RA chimeras after IL-2 treatment ranged between 15 and 43% and for IgM between 50 and 98% during 2-8 weeks postengraftment. Human IgM-RF was detectable after 1 to 2 weeks after engraftment and persisted over a period of 10-13 weeks. No RF was produced in SCID mice engrafted with PBMC from healthy individuals with or without exogenous rIL-2 administration. Thus, human rIL-2 expanded autoreactive clones involved in the production of RF in the SCID-RA chimeras. The present study provides a novel approach to establish an in vivo SCID-RA model to study the cellular and molecular mechanisms involved in the production of RF and development of a RA-like lesion.

Adult↗
PubMed1998

Expression of 70-kDa heat-shock protein during acute graft-versus-host disease.

Acute lethal graft-versus-host disease (GVHD) was induced in unirradiated (LEW x DA)F1 rats by injection of DA parental lymphoid cells. Control rats received the same dose of (LEW x DA)F1 cells. The level of hsp70 at different stages of GVHD was examined in the spleen, lymph nodes, thymus, liver, lung, kidney, heart, and skeletal muscles of GVHD and control animals. Hsp70 was present in all organs analyzed in both groups and, with the exception of the spleen and lymph nodes, detectable levels remained constant during the disease. However, the spleen and lymph nodes of GVHD rats showed distinct changes in the hsp70 levels throughout the course of the disease. Expression of hsp70 in spleen and lymph nodes was augmented 7 and 14 days after induction of the disease. During the last stages of GVHD, 18-21 days after the induction, expression of hsp70 diminished to a level similar to that in untreated and control animals. Elevated levels of hsp70 in lymphoid organs during GVHD suggest an involvement of hsp70 in the pathology of the disease.

Acute Disease↗
PubMed1994

Development of human lymphocyte-engrafted SCID mice as a model for immunotoxicity assessment.

Mice with the severe combined immunodeficient (SCID) and triple-deficient (bg/nu/xid) mutations lack select populations of functional immune cells. Studies by several laboratories have demonstrated the ability to restore certain missing immune components in these mice by reconstituting with various lymphoid tissues including peripheral blood lymphocytes (PBL) from mice and humans. Such a model could provide an opportunity to examine human lymphoid cells in an in vivo environment for immunotoxicity assessment. In the present studies, bg/nu/xid and SCID mice were reconstituted by intraperitoneal or intravenous injection with either tetanus-immunized syngeneic mouse splenocytes (mo-SPL) or tetanus-immunized human PBLs (hu-PBL) under various test conditions. Hu-PBL-SCID mice from the C.B-17 strain produced more successful human engraftments than mice from the bg/nu/xid or C3H-SCID strains. Using optimal conditions, mo-SPL-SCID and hu-PBL-SCID mice were engrafted and administered either 2,3,7,8-tetrachlorodibenzo-p-dioxin or cyclosporin A (Cys A) and periodically bled to measure tetanus-specific antibody and class-specific immunoglobulin concentrations. Comparison of the chemical-related changes in immunoglobulin and tetanus antibody concentrations revealed some similarities between control mice and mo-SPL-SCID or hu-PBL-SCID mice, particularly with Cys A groups. However, under the various conditions examined, hu-PBL-SCID mice demonstrated considerable variability in their ability to provide consistent reconstitution, thus, limiting the ability to determine whether human cells are more or less susceptible than mouse cells to the test agents. Provided that this system can be refined to provide consistent reconstitution, hu-PBL-SCID mice may be a promising in vivo model for assessment of potential immunotoxic agents.

Animals↗
PubMed2002

The role of tissue transglutaminase (transglutaminase type II) for the intestinal manifestations of murine semi-allogenic graft-versus-host disease.

The intestinal manifestation of acute murine semi-allogenic graft-versus-host (GvH) disease is characterized by the occurrence of lymphocytic infiltrates in the lamina propria, by crypt hyperplasia and villous atrophy. In a histological respect, this animal model resembles human celiac disease. Tissue transglutaminase (tTG) (transglutaminase type II) has been identified to be the major B cell autoantigen in celiac disease. Furthermore, tissue transglutaminase has been implicated to be involved in its pathogenesis. Therefore, we aimed to investigate whether tissue transglutaminase is expressed in the intestines of GvH animals and whether its inhibition has any effect on the intestinal histology. Sera of patients with celiac disease and anti-tTG antibodies were purified. These antibodies were used for immuno-histochemistry of jejunal cryosection from GvH and syngenic control animals at day 6 after lymphocyte transfer. Furthermore, GvH mice were treated with antitTG antibodies and with the inhibitor of tissue transglutaminase monodansyl-cadaverine. The effect of this treatment on the development of crypt hyperplasia and villous atrophy were examined by light microscopy of hematoxylin-eosin (H&E) stained jejunal paraffin sections. We found a strong subepithelial expression of tissue transglutaminase in GvH animals but not in syngenic control mice. The localization of tTG seemed to be associated with the extracellular matrix (ECM). However, neither the treatment of GvH animals with anti-tTG antibodies nor the application of mono-dansyl-cadaverine prevented the development of crypt hyperplasia and villous atrophy. Similar to the situation in human celiac disease tissue, transglutaminase is highly expressed in the intestine of animals undergoing a semi-allogenic graft-versus-host reaction. However, this enzyme is probably not involved in the development of crypt hyperplasia and villous atrophy in this animal model.

Animals↗
PubMed1993

Engraftment of bovine leukemia virus infected lymphocytes into SCID mice.

SCID mice inoculated with peripheral blood lymphocytes from a tumor-bearing BLV-positive cow developed lymphosarcomas after 6 months. DNA from the splenic tumor specifically hybridized with a bovine Sstl satellite probe, showing that these tumor cells were of bovine origin. The clonality of the SCID splenic tumor, as measured by the integration pattern of BLV proviruses, was the same as that in the donor lymphocyte population.

Animals↗
PubMed1997

The KSHV/HHV8-infected BCBL-1 lymphoma line causes tumors in SCID mice but fails to transmit virus to a human peripheral blood mononuclear cell graft.

The body-cavity-based lymphoma cell line BCBL-1, which is infected with Kaposi's sarcoma-associated herpesvirus/human herpesvirus 8, was injected alone or with human peripheral blood mononuclear cells into SCID mice. Immunoblastic lymphomas developed at or near the site of injection. The lymphomas appeared to derive exclusively from the injected BCBL-1 cells and not from the injected human PBMC. The tumors elicited a marked murine angiogenic response, but known angiogenic cytokines were not detected in BCBL-1 cells. Transfer of BCBL-1 cells to SCID mice may represent an in vivo model for the study of KSHV/HHV8-stimulated angiogenesis.

Animals↗