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At least 541 records · Page 30Linked to original sources
PubMed1976

The interplay between target organ concentrations of lymphocytic choriomeningitis virus and cell mediated immunity in baby mice.

Circumstantial evidence has been presented which supports the view that the fatal LCM virus infection is due to an immunological conflict in the host animal. Hitherto, this outcome of the infection has only been observed in intracerebrally infected mice. In the present study, the intraperitoneal infection in young mice was investigated and the results revealed a new example of this immunological conflict. In mice infected a few days after birth, concentrations of the virus in the brain are high, while the CMI response is non-measurable. If the infection is induced when the mice are 28 days old or more, there is little virus in the CNS, but a strong CMI response can be demonstrated. All the mice in these two age groups survive. If mice are infected when they are 17-19 days old, however, they raise a moderate CMI response nine days after infection and, at the same time, their brains contain virus in high titres. The mortality among mice infected at this age is 100%, indicating that this combination is fatal. The lives of these animals can be saved by anti theta serum or if they are transplanted with syngeneic lymphoid cells sensitized to LCM virus. Our results strongly suggest an interplay between, on the one hand, the spread and the magnitude of the virus infection in the brain and, on the other, the cell mediated immune response. This interplay seems to be decisive for the clinical outcome of the LCM infection in mice.

Age Factors↗
PubMed1977

Local lymph node response in rats to allogeneic stimulus: analysis of the in vitro responding cells.

Parental strain rats were immunized in the footpads by F1 hybrid spleen cells. The draining lymph nodes were removed during the first 10 days after immunization and tested for mitogen responsiveness. Cell fractionation was performed by removal of macrophages, surface Ig positive, and F(c)-, and C3-receptor carrying lymphocytes. The depleted suspensions were tested in MLC to test the effect of lymphocyte subpopulations on the accelerated MLC response profile exhibited by the immune lymph node cells. Overall increase in mitogen stimulation was observed, but stimulation indices were slightly reduced as compared to non-immunized cells. Removal of phagocytic cells gave some increase in MLC response which was most pronounced when responder cells were tested during the first days after immunization. Depletion for non-T lymphocytes resulted in lowering of non-stimulated responder cell 14C uptake, whereas the specific accelerated MLC profile was unaltered or tended to improve acceleration. It is concluded from indirect evidence that T lymphocytes are the cell type responsible for the altered MLC kinetics, but that macrophages and non-T cells modify the response.

Animals↗
PubMed1984

Immune responses to Legionella pneumophila in athymic nude rats.

Athymic nude rats (rnu) were immunized intraperitoneally with the attenuated Phil I strain (serogroup 1) of Legionella pneumophila. These rats developed a humoral immune response, including the IgG class, that was of comparable magnitude to that seen in their non-nude littermates. When the rats were challenged ip with a dose of the virulent strain LD-8 (also serogroup 1) that proved to be lethal in non-immune rnu-rats, none of them developed any signs of disease, but survived well for the observation period of 2 weeks. However, it was impossible by adoptive transfer of lymphocytes from immunized inbred PVG donors to protect non-immune syngeneic rats from the lethality of the LD-8. These results together with previous data (16) indicate that specific antibodies, present in the animal at the time of infection, protect effectively against a lethal dose of L. pneumophila in this experimental system.

Agglutination Tests↗
PubMed1999

The immune response to apoptotic cells.

Programmed cell death (PCD) can be divided into two distinct but linked sequential processes, killing of the cells and removal of the dead cells, which may be a neighboring cell or a professional phagocyte. Following internalization of the apoptotic cell, the phagocyte typically triggers neither the development of a pro-inflammatory response nor the production of autoantibodies directed against apoptotic self antigens. Since apoptotic cells are characterized by translocation of autoantigens such as nucleosomes to the surface of the cell, we tested the hypothesis that excess or abnormally processed apoptotic cells can generate autoantibodies. We have found that syngeneic apoptotic load can induce transient hypergammaglobulinemia, anti-DNA, anticardiolipin, and glomerular depositions in normal mice. Furthermore, we also found that one of the important mechanisms of uptake of apoptotic cells involves opsonization by the complement system, suggesting that deficient states could lead to aberrant handling of apoptotic cells. Therefore, conditions in which apoptotic cells become immunogenic may explain antigen selection in inflammatory and autoimmune conditions, such as in systemic lupus erythematosus (SLE).

Animals↗
PubMed1991

An in vivo model of somatic cell gene therapy for human severe combined immunodeficiency.

Deficiency of adenosine deaminase (ADA) results in severe combined immunodeficiency (SCID), a candidate genetic disorder for somatic cell gene therapy. Peripheral blood lymphocytes from patients affected by ADA- SCID were transduced with a retroviral vector for human ADA and injected into immunodeficient mice. Long-term survival of vector-transduced human cells was demonstrated in recipient animals. Expression of vector-derived ADA restored immune functions, as indicated by the presence in reconstituted animals of human immunoglobulin and antigen-specific T cells. Retroviral vector gene transfer, therefore, is necessary and sufficient for development of specific immune functions in vivo and has therapeutic potential to correct this lethal immunodeficiency.

Adenosine Deaminase↗
PubMed1995

Gene therapy in peripheral blood lymphocytes and bone marrow for ADA- immunodeficient patients.

Adenosine deaminase (ADA) deficiency results in severe combined immunodeficiency, the first genetic disorder treated by gene therapy. Two different retroviral vectors were used to transfer ex vivo the human ADA minigene into bone marrow cells and peripheral blood lymphocytes from two patients undergoing exogenous enzyme replacement therapy. After 2 years of treatment, long-term survival of T and B lymphocytes, marrow cells, and granulocytes expressing the transferred ADA gene was demonstrated and resulted in normalization of the immune repertoire and restoration of cellular and humoral immunity. After discontinuation of treatment, T lymphocytes, derived from transduced peripheral blood lymphocytes, were progressively replaced by marrow-derived T cells in both patients. These results indicate successful gene transfer into long-lasting progenitor cells, producing a functional multilineage progeny.

Adenosine Deaminase↗
PubMed1995

T lymphocyte-directed gene therapy for ADA- SCID: initial trial results after 4 years.

In 1990, a clinical trial was started using retroviral-mediated transfer of the adenosine deaminase (ADA) gene into the T cells of two children with severe combined immunodeficiency (ADA- SCID). The number of blood T cells normalized as did many cellular and humoral immune responses. Gene treatment ended after 2 years, but integrated vector and ADA gene expression in T cells persisted. Although many components remain to be perfected, it is concluded here that gene therapy can be a safe and effective addition to treatment for some patients with this severe immunodeficiency disease.

Adenosine Deaminase↗
PubMed1997

HSV-TK gene transfer into donor lymphocytes for control of allogeneic graft-versus-leukemia.

In allogeneic bone marrow transplantation (allo-BMT), donor lymphocytes play a central therapeutic role in both graft-versus-leukemia (GvL) and immune reconstitution. However, their use is limited by the risk of severe graft-versus-host disease (GvHD). Eight patients who relapsed or developed Epstein-Barr virus-induced lymphoma after T cell-depleted BMT were then treated with donor lymphocytes transduced with the herpes simplex virus thymidine kinase (HSV-TK) suicide gene. The transduced lymphocytes survived for up to 12 months, resulting in antitumor activity in five patients. Three patients developed GvHD, which could be effectively controlled by ganciclovir-induced elimination of the transduced cells. These data show that genetic manipulation of donor lymphocytes may increase the efficacy and safety of allo-BMT and expand its application to a larger number of patients.

Bone Marrow Transplantation↗
PubMed1988

Prevention of type I diabetes in nonobese diabetic mice by virus infection.

The nonobese diabetic (NOD) mouse is an animal model of type I diabetes and develops a characteristic autoimmune lesion in the islets of Langerhans with lymphocytic infiltration and destruction of pancreatic beta cells. The result is hypoinsulinemia, hyperglycemia, ketoacidosis, and death. Diabetes usually begins by the sixth month of age but can occur earlier when young NOD mice are infused with lymphocytes from older NOD donors. When newborn or adult NOD mice were infected with a lymphotropic virus they did not become diabetic. The interaction between viruses and lymphocytes is pivotal in aborting diabetes, as established by experiments in which lymphocytes from virus-infected donors failed to transfer diabetes. In contrast, lymphocytes from age- and sex-matched uninfected donors caused disease. Therefore, viruses and, presumably, their products can be developed to be beneficial and may have potential as a component for treatment of human diseases. Further, these results point to the utility of viruses as probes for dissecting the pathogenesis of a nonviral disease.

Animals↗
PubMed1976

Lymphocyte-induced angiogenesis in tumor-bearing mice.

The presence of a growing tumor can lead to a significant curtailment of a graft-versus-host reaction as measured by the ability of allogeneic spleen cells to induce a host vascular response. This interference with the normal pattern of immunological reactions may be a reason for the survival of tumors in an immunologically alien environment.

Animals↗
PubMed1975

T lymphocyte function as the principal target of lymphocytic choriomeningitis virus-induced immunosuppression.

Plaque-forming cell responses against sheep erythrocytes, Escherichia coli lipopolysaccharide, pneumococcal polysaccharide, and polyvinylpyrrolidone were examined in mice infected with lymphocytic choriomeningitis virus. A 92 to 96 percent reduction of the thymus-dependent anti-sheep erythrocyte responses was observed 2 to 4 weeks after infection. However, the thymus-independent responses against the three other antigens were close to normal at all stages of the infetion. Studies on allograft immunity of infected C3H mice against DBA/2 mastocytoma cells revealed a severe suppression of the T cell-mediated cytotoxic response which was temporally related to the impaired humoral responsiveness against sheep erythrocytes. The capacity of spleen cells from infected mice to restore immune responsiveness of lethally irradiated recipients against sheep erythrocytes was significantly reduced. The adoptive responses, however, were clearly improved when normal thymus cells were added to the inferior spleen cells. Moreover, it appeared that the spleen cells from immunosuppressed donor mice could not confer suppression to normal lymphoid cells. The presented findings are consistent with the assumption that a numeric deficiency of T cells, or cells belonging to some T cell subpopulation, is the primary cause of lymphocytic choriomeningitis virus-induced immunosuppression.

Animals↗
PubMed1975

Role for cell-mediated immunity in the resistance of mice to subcutaneous herpes simplex virus infection.

The role of cell-mediated immunity in the resistance of young adult mice to subcutaneous herpes simplex virus (HSV) type I infection was studied in mice receiving immunosuppressive doses of antilymphocyte sera (ALS) or antithymocyte sera (ATS). The effectiveness of these treatments to reduce cell-mediated responses was measured by their ability to prolong the life of allografts transplanted to ALS- or ATS-treated mice. It was found that subcutaneous infection of these mice with HSV resulted in spread of virus from the site of inoculation to the central nervous system. Neutralizing antibody could not be detected in the sera of ALS- or ATS-treated mice after HSV inoculation. Passive transfer of neutralizing antibody to ATS-treated mice did not restore resistance to subcutaneous HSV infection. However, adoptive transfer of HSV-sensitized spleen cells did provide significant protection against infection unless the spleen cells were treated with ATS prior to transfer. These experiments suggest that lymphocytes are involved in a cell-mediated response to subcutaneous HSV infection and demonstrate the importance of a noncompromised immune response in controlling spread of HSV from localized areas of infection.

Animals↗
PubMed1984

Characteristics of lymphoid cells that adoptively transfer immunity to Rickettsia mooseri infection in mice.

The capacity of adoptively transferred immune lymphoid cells or passively transferred immune serum to alter the course of an established Rickettsia mooseri (R. typhi) infection in the spleen was evaluated in BALB/c mice. Immune cells, but not immune serum, controlled the established infection. An effective lymphocyte was a T-cell which had to possess a capacity to divide.

Animals↗
PubMed1989

Modulation of macrophage Ia expression by lipopolysaccharide: stem cell requirements, accessory lymphocyte involvement, and IA-inducing factor production.

The mechanism of induction of murine macrophage Ia expression by lipopolysaccharide (LPS) was studied. Intraperitoneal injection of 1 microgram of LPS resulted in a 3- to 10-fold increase in the number of IA-positive peritoneal macrophages (flow cytometry and immunofluorescence and a 6-to 16-fold increase by radioimmunoassay. The isolated lipid A moiety of LPS was a potent inducer of macrophage Ia expression. Ia induction required a functional myelopoietic system as indicated by the finding that the response to LPS was eliminated in irradiated (900 rads) mice and reinstated by reconstitution with bone marrow cells. Comparison of LPS-induced Ia expression in normal and LPS-primed mice revealed a faster secondary response to LPS. The memory response could be adoptively transferred to normal mice with nonadherent spleen cells prepared 60 days after LPS injection. Spleen cells prepared 5 days after LPS injection caused Ia induction in LPS-nonresponder mice; such induction was not observed in irradiated (900 rads) recipients. The cell responsible for this phenomenon was identified as a Thy-1+, immunoglobulin-negative nonadherent cell. The biosynthesis and expression of Ia were not increased by direct exposure of macrophages to LPS in vitro. Small amounts of LPS inhibited Ia induction by gamma interferon. LPS showed positive regulatory effects on Ia expression by delaying the loss of Ia expression on cultured macrophages and by stimulating the production of Ia-inducing factors. Supernatants from cultured spleen cells stimulated with LPS in vitro contained antiviral and Ia-inducing activity that was acid labile, indicating that the active factor is gamma interferon. We conclude that induction of Ia expression by LPS in vivo is a bone-marrow-dependent, radiation-sensitive process which involves the stimulation of a gamma interferon-producing accessory lymphocyte and a delay in Ia turnover.

Animals↗
PubMed1973

Relationship of BCG-induced pulmonary delayed hypersensitivity to accelerated granuloma formation in rabbit lungs: effect of cortisone acetate.

The role of local pulmonary delayed hypersensitivity in accelerated pulmonary granuloma formation was investigated using cortisone acetate, an immunosuppressive drug that appears to preferentially eliminate committed lymphocytes at appropriate doses. Data are presented showing that cortisone acetate suppressed local pulmonary delayed hypersensitivity at the time of and subsequent to challenge with BCG. Furthermore, cortisone damage appeared to involve primarily committed lymphocyte populations since the defect was repairable with sensitized spleen cells, an unlikely source of macrophage precursors.

Animals↗