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At least 289 records · Page 16Linked to original sources
PubMed1982

Role of neutralizing antibodies and T-cells in pathogenesis of herpes simplex virus infection in congenitally athymic mice.

Congenitally athymic nude mice were infected with 10(4) p.f.u. herpes simplex type 1 (strain SC16). Following the passive transfer of neutralizing monoclonal antibodies (AP7, AP8 and AP12) it was observed that AP7 alone reduced the virus infectivity in the nervous system; AP8 and AP12 failed to protect mice probably due to poor in vivo binding to the neutralization site on the virus. Latent ganglionic infection could be established in nude mice following adoptive transfer of optimum number (2 x 10(7) cells/mouse) of immune lymph node cells from day 7 herpes virus-infected hairy immunocompetent donor mice. Moreover, in some of the immune lymph node cell protected nudes, latency could be maintained even in complete absence of neutralizing antibodies. Results of ear-ablation experiments revealed that removal of primary source of infection after day 5 of infection reduced the amount of virus in the ganglia and spinal cord. Acute neurological infection was not detected following transfer of protective anti-gp-D neutralizing antibody (LP2) in combination with removal of infected pinna. These data suggest that continuous seeding of virus occurs in related ganglia via the axonal route from infected ear pinna. It appears that local T-cell-mediated immune mechanisms are involved in maintenance of latency.

Animals↗
PubMed1985

Graft-versus-host disease in murine bone marrow transplantation. I. Modification of GVHD by preimmunization of recipients with spleen cells of primary recipients undergoing GVHD.

Lethally irradiated (1000 rad) CBA/J mice were transplanted with anti-Thy 1 treated BALB/c bone marrow. Under these conditions, we uniformly observed the development of pathology suggestive of acute graft-vs.-host disease (GVHD), i.e. weight loss, diarrhoea, hypogammaglobulinemia and thymic hypoplasia. If, 2 wk before irradiation, the recipients were preimmunized with spleen cells taken from mice undergoing acute GVHD, these symptoms were avoided. Instead, such animals seemed to show long term survival either with or without signs of chronic GVHD (hypergammaglobulinemia, splenomegaly, lymphoid hyperplasia). The ability to show long term survival with bone marrow allografts was dependent upon successful immunization of the recipient mice. Long term survivors contain a splenic population not bearing detectable host MHC antigens, which can elicit a memory anti-host cytotoxic response from a population of quiescent donor lymphocytes previously immunized in vitro against host MHC antigens.

Animals↗
PubMedDate not supplied

Attempts to transfer experimental allergic neuritis with lymphocytes.

Attempts have been made to transfer experimental allergic neuritis (EAN) both by the intraneural and the intravenous injection of cells derived from Lewis rats with the disease into naive recipients of the same strain. Lymph node cells obtained 12 and 15 days after inoculation with bovine dorsal root in Freund's complete adjuvant were injected intraneurally. A small number of demyelinated axons were observed, but clinical weakness was not evident. Lymph node cells, lymph node cells cultured with concanavalin A, or cultured spleen cells from animals with EAN were transferred intravenously to normal rats. Uncultured lymph node cells were transferred to X-irradiated animals. There were no clinical or histological differences between these recipients and controls receiving cells from rats inoculated with Freund's adjuvant alone. The findings are discussed in relation to previous reports of attempts to transmit EAN by cell transfer.

Animals↗
PubMed1988

Replication of donor lymphocytes in recipients is not essential for the passive transfer of allergic encephalomyelitis.

Gliotoxin is a fungal metabolite belonging to the class of epipolythiodioxopiperazines which possesses both immunomodulating and anti-phagocytic activities. We have examined the effect of gliotoxin on passively induced allergic encephalomyelitis and report here that pulse treating activated experimental allergic encephalomyelitis (EAE) effector lymphocytes with gliotoxin inhibits, in a dose-dependent manner, their ability to transfer disease. Cells treated with 300 ng/ml are unable to replicate in vitro in response to concanavalin A stimulation, nor did they produce interleukin-2 (IL-2) following stimulation. Furthermore this concentration of gliotoxin also causes complete fragmentation of genomic DNA in treated cells, yet these cells are still capable of transferring clinical EAE. These data suggest that replication of donor lymphocytes in the recipient is not essential for the development of EAE.

Animals↗
PubMed1989

Lymphocyte-myelin sheath interactions in acute experimental allergic encephalomyelitis.

Using a passively transferred acute model of experimental allergic encephalomyelitis (EAE) in the rat, inflammatory central nervous system (CNS) lesions were shown to develop rapidly, peak and then resolve. An unusual feature of the lesions in the CNS was the presence of pyknotic cells within myelin sheaths. A sequence of observations indicated that such cells were lymphocytes which had insinuated themselves into the myelin sheath by passage along the interperiod line. The presence of lymphocytes within myelin sheaths, a process which did not lead to demyelination, was considered to represent a change which reflects the specificity of the immune response in this disease. The detection of this change in other CNS autoimmune diseases, notably those associated with virus infections, may be important as an indicator of pathogenetically relevant lymphocyte-myelin interactions.

Acute Disease↗
PubMed1989

Demyelination and early remyelination in experimental allergic encephalomyelitis passively transferred with myelin basic protein-sensitized lymphocytes in the Lewis rat.

Histological studies were performed on Lewis rats with experimental allergic encephalomyelitis (EAE) passively transferred by myelin basic protein (MBP)-sensitized syngeneic spleen cells in order to determine the relationship between demyelination and neurological signs. Neither inflammation nor demyelination was present on the day prior to the onset of neurological signs but both were present in the spinal roots and spinal cord on the day of onset of tail weakness (4 days after passive transfer). Demyelination and the neurological signs both increased over the next 48 h. There was evidence that the caudal roots were more severely affected than the rostral roots. The peripheral nerves were spared. Demyelination in the spinal cord was concentrated in the dorsal root entry and ventral root exit zones. The initial stages of repair of demyelinated spinal root fibres by Schwann cells were observed on the earliest day that clinical recovery commenced (day 7). At this time some demyelinated fibres were closely associated with debris-free Schwann cells, and occasional fibres were completely invested by 1-2 layers of Schwann cell cytoplasm. Remyelination (compact myelin lamellae formation) by Schwann cells was first observed in the spinal roots on day 9. By the time of complete clinical recovery (day 11) the majority of affected spinal root cores had thin new myelin sheaths. Repair of central nervous system myelin by oligodendrocytes was slower than peripheral nervous system myelin repair. Investment of demyelinated spinal cord axons by oligodendrocytes was observed on day 9, and remyelination by these cells was seen on day 10. We conclude that the neurological signs of passively induced MBP-EAE can be accounted for by demyelination of the lumbar, sacral and coccygeal spinal roots and spinal cord root entry and exit zones, and that the subsequent clinical recovery can be explained by investment and remyelination of demyelinated peripheral and central nervous system fibres by Schwann cells and oligodendrocytes respectively.

Animals↗
PubMed1992

Concordance and localization of maximal vascular permeability change and fibrin deposition in the central neuraxis of Lewis rats with cell-transferred experimental allergic encephalomyelitis.

This study utilized Lewis rats and the cell-transfer form of experimental allergic encephalomyelitis (EAE) to focus on two central nervous system microvascular alterations known to be intimately associated with early clinical neurological signs of the disease, namely increased vascular permeability and deposition of fibrin. The main objective of the work was to define the degree of concordance and the anatomical localization of maximal vascular permeability change and fibrin deposition within the neuraxis of recipient rats during the earliest expression of clinical manifestations of the disease. Recipients were injected with predetermined doses of activated, myelin basic protein (MBP)-reactive syngeneic donor lymphoid cells and killed 6 or 7 days later when they exhibited the first clinical signs of disease. This experimental design allowed assessment of late occurring immune activities of a single population of MBP-reactive effector cells. Increased vascular permeability, expressed as mean extravascular blood equivalents (EVBE), attained maximum change, i.e., 16.04 +/- 5.07, within the lumbosacrococcygeal segment of the spinal cord (LSC). Maximal density of fibrin depositions, i.e., 192 +/- 94 deposits, also occurred within the LSC cord. The concordance of these two histoimmunopathological events, their tight linkage to early clinical signs of disease and the fact that both events attained maximal values within the LSC cord suggest that increased permeability and activation of the coagulation cascade may be prerequisite events for the expression of neurological signs of EAE.

Animals↗
PubMed1994

Adoptive transfer of experimental allergic encephalomyelitis: recipient response to myelin basic protein-reactive lymphocytes.

We have used adoptive transfer of myelin basic protein (MBP)-reactive lymphocytes in the Lewis rat model of experimental allergic encephalomyelitis (EAE) to identify stages of effector cell development and to investigate the nature of the subsequent recipient response to the transferred cells. Depending on the timing of cell collection, lymph node cells (LNC) obtained from MBP-CFA (MBP emulsified in complete Freund's adjuvant)-immunized donors may directly transfer clinical disease; however, independent of disease development, recipients of LNC develop early onset of clinical disease following immunization of the recipients with MBP-CFA, consistent with the presence of MBP-memory cells in the LNC transfer inoculum. Similarly obtained spleen cells do not directly transfer disease and do not contain MBP-memory cells (as defined by the early onset of clinical disease following MBP-CFA challenge). Spleen cells adoptively transfer clinical disease only following in vitro culture stimulation with antigen or selected mitogens. Recipients of the primary culture-derived encephalitogenic spleen cells also develop an accelerated onset of clinical disease following MBP-CFA challenge, indicative of the presence of MBP-memory cells, and are not vaccinated. Encephalitogenic T cell lines adoptively transfer clinical disease, and in most cases recipients are vaccinated to MBP-CFA-induced active disease, but remain susceptible to adoptively transferred disease. Co-transfer of encephalitogenic T cell line cells with MBP-reactive lymph node or encephalitogenic spleen cells does not alter the vaccination response. We have found that during the process of T cell line development, the vaccinating phenotype is acquired following the second antigen stimulation cycle. These studies also demonstrate that regulation induced by T cell vaccination blocks the development of effector cells from precursor cells and that such regulation is also equally effective in blocking disease development in recipients which have increased numbers of memory cells. Thus, the response to T cell vaccination, once established, is fully capable of inhibiting the development of effector cells from increased numbers of precursor/memory cells, a response that would be needed in the clinical application of vaccination-induced resistance.

Animals↗
PubMed1984

Rationale for a novel immunotherapy of cancer with allogeneic lymphocyte infusion.

A simple method of cancer immunotherapy has been developed which achieves marked objective response in 20-30% of patients with disseminated disease. Each course consists of a low dose of chemotherapy followed two days later by intravenous infusion of allogeneic lymphocytes. Courses are repeated on a monthly basis as needed. The function of the chemotherapy--too mild to significantly influence tumor growth directly--appears to be depletion of suppressor T cells, which sensitizes the patient to the immunostimulant action ("allogeneic effect") of the subsequently infused lymphocytes. The rationale for this method is discussed in the context of a review of past attempts at lymphocyte immunotherapy. We are now attempting to improve response rates by combatting anergy with nutritional immunopotentiators, and by preventing prostaglandin-mediated or -dependent immunosuppression with prostaglandin synthetase inhibition. By understanding and counteracting the various specific and general means by which a growing tumor induces host tolerance, it should prove possible to achieve immune-mediated tumor regression in a high proportion of patients. Best results may be seen when allogeneic lymphocyte therapy is initiated at an earlier stage of the disease, and is used in conjunction with surgery, radiotherapy, short-course intensive chemotherapy, or hyperthermia-based methods.

Combined Modality Therapy↗
PubMed1984

Reconstitution of immunosuppression mice with mononuclear cells from donors sensitized to foot-and-mouth disease virus (FMDV).

Passive transfer experiments were performed to serve as a basis for analyzing the immune response of adult mice to FMDV infection. Animals were irradiated (750 rad: 1 lethal dose 50%) and reconstituted with allogeneic mononuclear cells from blood, spleen, thymus and peritoneal cavity from donors 2 and 8 days post-inoculation (p.i.). Donors were primed with 10 000 suckling mouse 50% lethal doses of FMDV strain O1 Campos. The following parameters were studied in recipient mice challenged with 10 000 suckling mouse 50% lethal doses of the same virus: (1) viremia; (b) FMDV neutralizing antibody titres; (c) sheep red blood cell (SRBC) hemagglutinating antibody titres. Viremia was substantially prolonged in irradiated control mice, which did not produce detectable antibodies to FMDV or SRBC. In contrast, the span of viremia was markedly shorter in animals reconstituted with cells obtained 8 days p.i. and its eclipse coincided with the onset of neutralizing antibody production. An equally efficient antibody response to the inoculation of SRBC was observed in these animals. No effect was detected after the transfer of cells obtained 2 days p.i. It is concluded that the humoral immune response plays a predominant role in the recovery from FMDV experimental infection in adult mice.

Animals↗
PubMed1985

An attempt to protect calves against experimental bovine leukosis using allografts.

Six calves sensitised by implanting skin from a calf were later inoculated with lymphocytes from the same calf after the calf had been infected with bovine leukosis virus (BLV). Two out of 6 calves challenged did not develop BLV antibodies and BLV was not isolated from these animals, whereas all of the 5 control calves became infected with BLV.

Animals↗
PubMed1989

Cancer therapy: it was by persisting that the Greeks took Troy.

A rather pessimistic wind is blowing over cancer chemotherapy, while a not very objective enthusiasm for second generation immunotherapy is raising its head. As the natural father of the first allogeneic bone marrow graft, of lymphocyte transfusions and of active immunotherapy, my duty is to show that chemotherapy is doing fine, and that the neo-immunotherapists would do well do draw some lesions from retrospective studies in their field, which might guide their approach towards efficient cancer (and AIDS) therapy.

Humans↗
PubMed1992

Recombinant human growth hormone promotes human lymphocyte engraftment in immunodeficient mice and results in an increased incidence of human Epstein Barr virus-induced B-cell lymphoma.

Recombinant human growth hormone (rhGH) previously has been demonstrated to promote human or mouse T-cell engraftment in immunodeficient mice. We then wanted to examine long-term effects of rhGH on human cell engraftment in these mice. Mice with severe combined immune deficiency (SCID) were given human peripheral blood lymphocytes or human bone marrow cells and daily injections of rhGH (20 micrograms ip every other day). Upon later assessment for engraftment by flow cytometric analysis, it was determined that rhGH strongly promoted human T-cell engraftment in the thymus and spleens of these mice. However, there was considerable variability in both the incidence and extent of engraftment which appears to be due to donor-to-donor variation. Additionally, rhGH promoted B lymphomagenesis in these mice since long-term treatment of these xenogeneic chimeras with rhGH resulted in the increased incidence of human Epstein-Barr virus (EBV)-infected B-cell lymphoma. Thus, while rhGH can be used to optimize human T-cell engraftment in SCID mice, it also increases the likelihood of B-cell lymphoma generation when the donor is EBV infected. The results suggest that the activation of human T cells by rhGH results in an increased ability of these cells to traffic to the peripheral lymphoid organs of the SCID mice and results in a lymphoid microenvironment conducive to the outgrowth of EBV-transformed B lymphocytes.

Animals↗
PubMed2006

CTLA-4.FasL inhibits allogeneic responses in vivo.

CTLA-4.Fas ligand (CTLA-4.FasL), a paradigmatic 'trans signal converter protein (TSCP)', can attach to APC (via CTLA-4 binding to B7) and direct intercellular inhibitory signals to responding T cells (via FasL binding to Fas receptor), converting an activating APC-to-T cell signal into an inhibitory one. Our previous studies established that CTLA-4.FasL inhibits human primary mixed lymphocyte reactions (MLR) and induces alloantigen-specific hyporesponsiveness ex vivo. The present study extends this to an in vivo context. Using splenocytes from MHC-mismatched C57BL/6 and Balb/c mice, we demonstrated that his(6)CTLA-4.FasL, effectively inhibits murine MLR. Moving in vivo, we demonstrated that subcutaneously administered his(6)CTLA-4.FasL modulates the in vivo response of infused allogeneic splenocytes. his(6)CTLA-4.FasL reduces the number of cells in each cell division, and increases the percentage of dead cells in each division. These findings are consistent with an antigen-induced cell death of the alloreactive cells, and bolsters recombinant TCSP promise as a therapeutic for transplantation diseases.

Adoptive Transfer↗
PubMed2005

Defective stromal cell function in a mouse model of infusion-induced bone marrow failure.

OBJECTIVE: To study bone marrow (BM) stromal damage in a mouse model of infusion-induced BM failure. MATERIALS AND METHODS: Sublethally irradiated CByB6F1 mice were infused with 5 x 10(6) C57BL/6 (B6) lymph node (LN) cells. Recipient BM cells were taken at 3, 7, 10, and 14 days following LN infusion and were cultured in vitro in alpha-modified Eagle media for 2-3 weeks. Peripheral blood and was analyzed by complete blood counts while BM lymphocyte infiltration/expansion was analyzed by flow cytometry. Marrow cells from affected and control mice were mixed and cultured in vitro to test nonspecific stromal damage. RESULTS: Donor lymphocytes infiltrated host BM within 3-7 days and expanded significantly between 7 and 10 days, concurrent with the development of leukopenia, thrombocytopenia, and marrow hypoplasia. BM cells from mice at 7, 10, and 14 days after B6-LN cell infusion were progressively defective in forming stromal feeder layers. A 1:1 mixture of BM cells from affected CByB6F1 mice and normal B6 mice failed to form an effective stromal feeder layer that could support cobblestone colony formation, indicating that lymphocytes in the BM of affected CByB6F1 mice were able to damage stromal cells in the normal B6 BM. CONCLUSION: Activated lymphocytes destroy both hematopoietic and stromal cells as innocent bystanders in the infusion-induced BM failure model.

Animals↗