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In vivo administration of histoincompatible lymphocytes leads to rapid functional deletion of cytotoxic T lymphocyte precursors.

It is well established that a single intravenous injection of F1 lymphocytes can rapidly and specifically reduce the ability of a parental recipient to generate CTL against donor alloantigens in a subsequent MLR. By fluorescently labeling the injected cells, we have been able to identify, and if desired, remove them in cell suspensions prepared from recipient spleen and lymph node. The injected cells, whether F1 or syngeneic, appeared to form part of the normal recirculating pool. Removal of injected F1 cells from responder lymph node or spleen cell suspensions had no effect on the response reduction observed in the 5-d in vitro MLR (typically 80% reduction for responder cells taken 2 d after injection of F1 cells). When the frequency of CTL precursors (CTLp) was measured by limiting dilution, it was reduced to the same degree as the MLR response, implying that response reduction is due to a reduction in the number of activatable CTL in the responder cell suspension. An equal mixture of responder cells from treated (i.e., F1 injected) and control mice gave a measured CTLp frequency equivalent to the average of the separate frequencies, implying the absence of suppressor cells active in vitro. Labeled F1 cells recovered from a first recipient could be used to induce response reduction in a second recipient. The results are discussed in terms of APCs that functionally delete rather than stimulate CTLp that recognize them (i.e., a "veto mechanism"). These experiments appear to rule out a role for in vivo-induced suppressor cells up to 8 d after injection of semiallogeneic cells but do not address the question of whether they are induced at later times.

Animals↗

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

Human PBL have been reported to reconstitute B and T cells as well as human serum Ig in mice with severe combined immunodeficiency disease (SCID). To confirm these observations and attempt the transfer of an autoimmune disease to the immunodeficient animals, groups of SCID mice received an injection of PBL from patients with primary biliary cirrhosis (PBC) or from normal volunteers. By 8 wk after the injection of 10-42 x 10(6) PBL into the mice, human lymphoid cells were detected in the spleen of approximately half of the animals and all had detectable serum levels of human IgG. Moreover, the sera of SCID mice that received cells from patients with PBC contained human antimitochondrial antibodies (AMA) to dihydrolipoamide acetyltransferase, the major mitochondrial autoantigen of PBC. Histologically, a human mononuclear cell infiltrate was present around the portal areas of the liver and inflammation, bile duct atypica, and necrosis of bile duct cells were observed. While the biliary lesions in the SCID recipients of PBC cells were more severe, a mononuclear infiltrate was clearly evident in mice that received cells from normal donors, suggesting the presence of a graft-vs.-host-like disease. While these data are the first to describe an animal model with both the humoral and cellular characteristics of PBC, they also raise an interesting question regarding the preferential localization of lymphoid cells to the biliary system.

Animals↗

Synergistic antitumor activity of tumor-infiltrating lymphocytes, interleukin 2, and local tumor irradiation. Studies on the mechanism of action.

The adoptive transfer of tumor-infiltrating lymphocytes (TIL) with the concomitant administration of IL-2 has been shown to mediate the regression of established 6- and 14-d murine hepatic and pulmonary metastases. For successful immunotherapy with TIL, however, pretreatment with either cyclophosphamide (CP) or whole body irradiation (WBX) was required. The exact mechanism of CP and WBX augmentation of TIL antitumor activity remains unknown, but the elimination of Ts cells has been frequently invoked as an explanation. To address this possibility and to determine if local tumor irradiation (LTX) could synergize with TIL as well as WBX, we investigated the effect of LTX on the therapeutic efficacy of TIL and IL-2 in the treatment of multiple 7-d murine hepatic metastases. Experiments studying the treatment of a weakly immunogenic murine adenocarcinoma, MC-38, showed prolonged survival of mice treated with the combination of IL-2, TIL, and either LTX or WBX, compared with treatment with radiation alone or radiation plus IL-2 controls (p less than 0.0001). In addition, therapy with LTX and IL-2 prolonged survival, compared with LTX administration alone, whereas therapy with WBX combined with IL-2 did not alter survival. This augmentation of TIL-mediated antitumor activity was dependent on the dose of radiation used. To assess the possibility that tumor-associated Ts cells inhibit the function of adoptively transferred TIL in animals with 7-d metastatic tumor and are eliminated by WBX and LTX, we repeated the above experiments leaving some tumor unirradiated. Mice underwent either LTX or limited LTX, which included only the right side of the liver (LTX1/2). The number of right- and left-sided metastases were then individually counted. These studies showed that the reduction in the number of right-sided metastases was identical between the two groups and that the presence of left-sided tumor in the LTX1/2 group did not suppress the observed antitumor activity of TIL against irradiated tumor. Additional evidence against the elimination of suppressor cells as an important mechanism in radiation-induced augmentation of TIL antitumor activity was provided by experiments studying the effectiveness of TIL in thymectomized, lethally irradiated, and reconstituted B mice. Unless CP was administered before the adoptive transfer of TIL, therapy with IL-2 and TIL in these B mice was ineffective in the absence of demonstrable T lymphocytes.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma↗

Correlation between lymphocyte-induced donor-specific tolerance and donor cell recirculation.

Intravenous infusion of mice with major histocompatibility complex (MHC) incompatible lymphocytes can inhibit the response of recipient T cells capable of recognizing the injected cells, and can enhance survival of grafts sharing MHC with the injected cells. However, neither T cell inactivation nor graft survival enhancement is always achieved. This is particularly true for donor cells that are fully allogeneic (as compared to semiallogeneic) to the recipient. We show here that both donor-specific induced response reduction and graft survival enhancement are directly correlated with the ability of the injected lymphoid cells to persist in the recirculating lymphocyte pool of the host. Whether donor cells persist correlates inversely with the level of natural killer cell (NK) activity in the host. Fully allogeneic cells can only persist in hosts with low NK activity and can then induce response reduction. Both persistence and response reduction are abrogated by injection of the host with poly-I:C, a treatment that boosts host NK activity. The same treatment also destroys the ability of semiallogeneic injected cells to persist, to induce response reduction, and to enhance skin graft survival.

Animals↗

Lymphoproliferative disease in human peripheral blood mononuclear cell-injected SCID mice. I. T lymphocyte requirement for B cell tumor generation.

Mechanisms of tumor development were studied in SCID mice injected with human lymphoid cells from Epstein-Barr virus-positive (EBV+) donors. About 80% of peripheral blood mononuclear cell (PBMC)-injected animals developed a lymphoproliferative disease associated with oligoclonal EBV+ tumors of human B cell origin. No change in tumor development rate occurred when monocyte-depleted PBMC were inoculated. No tumors developed when purified B cells were injected. B cell lymphoproliferative disease was also prevented in most cases when PBMC-injected animals were treated with agents that prevent T cell activation, such as cyclosporin A. Both CD4+ and CD8+ T cell subpopulations were able to provide putative factor(s) necessary for EBV+ B cell expansion and progression to tumors. These data suggest that the transfer alone of potentially tumorigenic human cells into an immunodeficient environment, such as the SCID mouse, might not be sufficient for cell progression to tumor, and raise the possibility that chronic activation events could play a major role in the pathogenesis of some EBV+ lymphomas in the immunocompromised host.

Adult↗

Potent immune response against HIV-1 and protection from virus challenge in hu-PBL-SCID mice immunized with inactivated virus-pulsed dendritic cells generated in the presence of IFN-alpha.

A major challenge of AIDS research is the development of therapeutic vaccine strategies capable of inducing the humoral and cellular arms of the immune responses against HIV-1. In this work, we evaluated the capability of DCs pulsed with aldrithiol-2-inactivated HIV-1 in inducing a protective antiviral human immune response in SCID mice reconstituted with human PBL (hu-PBL-SCID mice). Immunization of hu-PBL-SCID mice with DCs generated after exposure of monocytes to GM-CSF/IFN-alpha (IFN-DCs) and pulsed with inactivated HIV-1 resulted in a marked induction of human anti-HIV-1 antibodies, which was associated with the detection of anti-HIV neutralizing activity in the serum. This vaccination schedule also promoted the generation of a human CD8+ T cell response against HIV-1, as measured by IFN-gamma Elispot analysis. Notably, when the hu-PBL-SCID mice immunized with antigen-pulsed IFN-DCs were infected with HIV-1, inhibition of virus infection was observed as compared with control animals. These results suggest that IFN-DCs pulsed with inactivated HIV-1 can represent a valuable approach of immune intervention in HIV-1-infected patients.

AIDS Vaccines↗

Donor lymphocyte infusion: the use of alloreactive and tumor-reactive lymphocytes for immunotherapy of malignant and nonmalignant diseases in conjunction with allogeneic stem cell transplantation.

Donor lymphocyte infusion (DLI), pioneered in Jerusalem in January 1987, represents the first proof of principle of the absolute efficacy of immunotherapy as a means of curing cancer. Immunotherapy with alloreactive donor lymphocytes can eliminate "the last tumor cell" even in patients with hematological malignancies resistant to maximally tolerated doses of chemoradiotherapy. Alloreactive lymphocytes that can mediate anti-tumor effects following induction of host-versus-graft tolerance induced by transplantation of donor stem cells, can induce graft-versus-malignancy (GVM) effects which are usually accompanied by graft-versus-host disease (GVHD). However, occasionally GVM effects may also be accomplished independently of clinically overt GVHD. Interestingly, allogeneic donor lymphocytes may also eliminate undesirable host-derived hematopoietic cells in a large number of nonmalignant indications including genetic diseases, diseases caused by deficiency of stem cell products, and autoimmune disorders mediated by self-reactive lymphocytes. The cumulative clinical experience suggests feasibility of effective induction of graft-versus-leukemia (GVL); graft-versus-lymphoma (GVLy); graft-versus-multiple myeloma, as well as graft-versus-solid tumors (GVT), well-documented in patients with renal and breast cancer, even in patients with resistant disease that have failed myeloablative chemoradiotherapy. These observations that suggested that cell therapy by donor lymphocytes is the main therapeutic benefit of bone marrow transplantation (BMT) led to development of the nonmyeloablative approach for safer allogeneic stem cell transplantation. Nonmyeloablative stem cell transplantation (NST) makes it possible to offer an option for cure to elderly patients with no upper age limit, as well as to patients with poor performance status not considered eligible for conventional BMT. Using well-tolerated NST regimen, allogeneic stem cell transplantation can be accomplished with minimal procedure-related toxicity and mortality, possibly even on an outpatient basis. Immunotherapy mediated by adoptive allogeneic cell-mediated immunotherapy can be further improved by utilizing specifically immune donor lymphocytes, thus maximizing their efficacy against undesirable target cells of host origin on the one hand, while minimizing their ontoward efficacy against normal cells of host origin that could result in GVHD on the other. Taken together, DLI and subsequently NST, may have opened new horizons for treatment of life-threatening malignant and nonmalignant disorders correctable by allogeneic stem cell transplantation. It is anticipated that further improvement of reactivity and specificity of donor lymphocytes will lead to safer clinical application of cell therapy for a larger number of indications toward improving disease-free survival in a large number of indications while minimizing immediate and late procedure-related complications.

Animals↗

Comparison of protection afforded by whole virus ISCOM versus MDP adjuvanted formalin-inactivated SIV vaccines from IV cell-free or cell-associated homologous challenge.

A SIV-ISCOM and a SIV-MDP adjuvanted vaccine were tested for their potential to induce protection from intravenous cell-free or cell-associated homologous SIV challenge in rhesus monkeys (Macaca mulatta). Seven monkeys vaccinated four times over a four-month period with either the SIV-ISCOM or the SIV-MDP vaccine were challenged intravenously with approximately 10 MID50 cell-free SIVmac251 (32H). They all were protected from developing viremia during a three-month observation period. Two other groups of four monkeys were vaccinated essentially in the same way with either of these vaccines. They were challenged intravenously with approximately 10 MID50 of infected PBMC of a rhesus monkey that had been infected with SIVmac251 (32H) 11 months earlier (stock prepared by J. Heeney). Two monkeys of each of these two groups proved to be protected from developing viremia during a two-month observation period. For both the cell-free and the cell-associated SIV challenge, monkeys vaccinated with measles virus ISCOMS or MDP adjuvanted measles virus antigen, served as controls. They all became viremic within two weeks after SIV challenge. This is the first demonstration that vaccinated previously unchallenged nonhuman primates can be protected from infection with lentivirus-infected PBMC from another animal. Serological analysis indicated that SIV-specific serum antibody titers were considerably higher in SIV-ISCOM vaccinated animals than in the SIV-MDP vaccinated animals. The serology also confirmed the protection data, by showing the absence of increase in SIV-specific serum antibodies in apparently protected animals after challenge.

Acetylmuramyl-Alanyl-Isoglutamine↗

Transfer of the ADA gene into bone marrow cells and peripheral blood lymphocytes for the treatment of patients affected by ADA-deficient SCID.

Severe combined immunodeficiency (SCID) caused by deficiency of the enzyme adenosine deaminase (ADA) is the first genetic disorder considered for human somatic cell gene therapy. ADA-SCID patients can be cured by HLA-matched sibling donor bone marrow transplantation. Alternative transplantation strategies as well as enzyme replacement are being tested in those patients who do not have a suitable matched sibling donor. Some ADA-SCID patients may not be candidates for cytoablation due to infectious damage to the lung or liver, or may have a milder phenotype that does not justify the risks associated with haploidentical bone marrow transplantation. Replacement therapy with PEG-ADA has resulted in improvement in growth, a variable increase in the number of peripheral blood lymphocytes, and a decrease in the incidence of severe infections. Another approach to the treatment of severe genetic diseases is now represented by somatic cell gene therapy. We and others have conducted experiments in vitro and in vivo that have documented that T-lymphocytes are suitable vehicles for gene transfer. Although the pluripotent stem cell remains the ideal target cell for somatic cell gene therapy of disorders of the hematopoietic system, the use of T-lymphocytes as gene therapy vehicles is specifically indicated for ADA-deficient patients where they represent the affected cells. Furthermore, the selective engraftment of T-cells only, following bone marrow transplantation, has resulted in reconstitution of cellular and humoral immunity. A model for the functional analysis in vivo of the human immune system has been utilized for the preclinical evaluation of this approach.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Deaminase↗

A controlled, Phase 1 clinical trial to evaluate the safety and effects in HIV-1 infected humans of autologous lymphocytes transduced with a ribozyme that cleaves HIV-1 RNA.

This Phase I study, "Ribozyme Gene Therapy of HIV-1 Infection" (UCSD HSC #971072, FDA BB-IND 6405), is a prospective, open-label trial of infusion of autologous gene-altered cells into asymptomatic HIV-1 seropositive individuals. The objectives of this trial are to test the safety, feasibility, and potential efficacy of T-cell ribozyme gene therapy of HIV-1 infection. To accomplish this, autologous CD8-depleted mononuclear cells are transduced with ribozyme expressing or control murine retroviral vectors, expanded ex vivo, and and infused. Subjects are monitored intensively to determine effects of infusion on HIV burden and replication. In addition, in vivo survival of control and ribozyme transduced cells is followed in an effort to obtain evidence of proof of concept. A unique strategy of sample blinding is introduced in this protocol, wherein both subject and control specimens are supplied to the research laboratory as coded samples, spiking blood from HIV seropositive volunteers matched for CD4 lymphocyte count with known but varying numbers of cells transduced with each vector. While this study is still in progress, preliminary results indicate that infusion of gene-altered, activated T-cells in HIV infected patients is safe, and that transduced cells can persist for long intervals in HIV-infected subjects. Results also suggest ribozyme transduced cells may possess a survival advantage in vivo.

Clinical Protocols↗

Immunologic effects of human peripheral and intrathyroidal lymphocytes on xenotransplanted human thyroid tissue in athymic nude mice.

T cells are intimately involved in the etiology and pathogenesis of human autoimmune thyroid disease. In order to further elucidate the immunologic mechanisms leading to Graves' disease (GD), we investigated the effects of human lymphocytes derived from patients with autoimmune and nonautoimmune thyroid diseases on human thyroid tissue xenotransplanted into nude mice. Eight weeks after transplantation of thyroid tissue from 26 patients with nonautoimmune thyroid disease (nontoxic nodular goiter [NTG]) into nude mice, peripheral (PBL) and intrathyroidal lymphocytes (ITL) from 14 patients with NTG and 12 patients with GD were engrafted into the animals. ITL and PBL subsets were analyzed by flow cytometer before engraftment. Two days after lymphocyte engraftment, the thyroid transplants were examined histologically (HE) as well as immunohistologically by staining with monoclonal antibodies directed against CD3 (T-cell activation and signal transduction), immunoglobulin G (IgG), HLA class II and CD31 (human endothelium). After injection of GD lymphocytes, thyroid transplants contained significantly more CD3, HLA class II, and CD4 expressing cells. Engrafted PBL and especially ITL from patients with GD specifically migrated into human thyroid transplants but not into the mouse thyroids, induced expression of class II products and led to IgG production by plasma cells. Persistence of human endothelium has been proven by positive CD31 staining. In conclusion, our data demonstrate that an organ-specific immune response is induced only by GD lymphocytes that migrate specifically into the thyroid transplants. Persistence of human endothelial cells in the transplants suggests that homing in this in vivo model reflects the situation in GD patients.

Adult↗

Toward an understanding of the mechanisms of classical conditioning of antibody responses.

Mice of different ages were subjected to repeated exposure to cyclophosphamide:saccharin (conditioned), or cyclophosphamide:saccharin followed by saccharin only (extinguished). Only young animals in the former group showed a decreased IgG antibody-forming-cell (AFC) response after challenge with sheep erythrocytes (SRBC) in the presence of saccharin. When irradiated conditioned young animals were used as recipients of antigen-challenged spleen cells from nonconditioned mice they were found to support a greater immune response than nonconditioned recipients. Similarly, cells from conditioned young mice gave a greater immune response in naive recipients than did cells from nonconditioned mice. Only when cells from conditioned young mice rather than conditioned "aged" mice were studied in irradiated conditioned young recipients was immunosuppression observed. These data are most consistent with a specific host cell:environment interaction being responsible for the conditioned immunosuppression observed in young mice. A deficit in both cells/environment apparently occurs during aging. At least one of these deficiencies seems related to loss of a suppressor T-cell population with age in conditioned mice.

Aging↗

Treatment with the alpha-glucosidase 1 inhibitor 6-O-butanoyl castanospermine reduces the detection of LFA-1 (CD18/CD11a) by monoclonal antibodies.

The antiviral clinical candidate 6-O-butanoyl castanospermine (MDL 28,574), an alpha-glucosidase 1 inhibitor, was examined for its effect on elementary parameters of immune function. It did not affect the mitogenic response of uninfected human mononuclear leukocytes or the detection of a range of cell surface markers, with the exception of the integrin LFA-1 (CD18/CD11a), which was reduced, after cell growth in vitro. The detection of LFA-1 was also reduced on both human and murine cells after oral administration of the compound to xenochimaeric or normal mice, respectively. Altered LFA-1 expression or function may contribute to reduced cell adhesion and the observed reduction in the in vitro allogeneic response by uninfected cells, as well as the previously described prevention of cell conjugate and HIV-induced syncytium formation.

Animals↗

Adverse effects of intradermal allogeneic lymphocyte immunotherapy: acute reactions and role of autoimmunity.

BACKGROUND: Immunotherapy with allogeneic lymphocytes was introduced as a therapeutic option for selected infertile couples in different centres worldwide 20 years ago. It has been suggested for other indications as well, e.g. for pregnant women at risk of a child with Rhesus-D haemolytic disease, or as a vaccine which might reduce the receptiveness for HIV-1 infection. Here we report on our experience on adverse side-effects of intradermal lymphocyte immunotherapy (LIT) for infertile couples using partner's lymphocytes. METHODS: Prospective 4 week follow-up of all couples from 2000 to 2003 for acute reactions (feedback 2687/3246 [corrected] 83%). All couples treated between 1996 and 2002 received questionnaires after 2-3 years (feedback 1914/3041, 63%). RESULTS: Local reactions predominantly consisted of redness and itching for approximately 2 weeks. Systemic reactions could be attributed to LIT in 6-8%. Blisters at the injection sites were characteristic of LIT but not dependent on the HLA class I mismatch status between cell donor and host. The incidence of autoimmune disease was 0.1%. Four patients developed thromboembolism in pregnancy which was not ascribed to antiphospholipid syndrome. CONCLUSIONS: Acute side-effects are comparable to those reported after intradermal vaccination for infectious diseases. Specific risks for anaphylaxis, autoimmune or graft versus host disease were not detected.

Adult↗

Host immune responses after administration of inactivated Venezuelan equine encephalomyelitis virus vaccines. II. Kinetics of neutralizing antibody responses in donors and adoptively immunized recipients.

Lymphoid cell responses to immunization with various formalin-inactivated Venezuelan equine encephalomyelitis (VEE) virus vaccines were monitored in mice by assessment of the development of both the neutralizing antibody response in sera of spleen cell donors and the adoptive neutralizing antibody response induced by spleen cell transfer in recipients. Donors immunized intraperitoneally with formalin-inactivated VEE vaccine (a single dose or a dose on three consecutive days) developed early serum neutralizing antibody responses (larger than or equal to 1:88-1:100) by seven days after immunization. Recipients of spleen cells from such mice were, however, incapable of eliciting a neutralizing antibody response (less than or equal to 1:10). Only spleen cells from donors immunized with inactivated VEE vaccine plus adjuvants (particularly complete Freund's adjuvant and Bordetella pertussis) were consistently capable of producing early, high-titer serum neutralizing antibody responses in adoptively immunized recipients (larger than or equal to 1:50-1:120 on day 4). The magnitude of neutralizing antibody responses of donors to inactivated VEE vaccines did not serve as a useful indicator of whether spleen cells from such mice could adoptively induce antibody responses in recipients. Finally, treatment of immune spleen cells with rabbit antiserum to mouse thymocytes, but not with rabbit antiserum to mouse gamma-globulin or normal rabbit serum, abolished the capacity of such cells to transfer an antibody response adoptively.

Adjuvants, Immunologic↗