PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Lymphocyte Transfusion”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources

Absence of RT6+ T cells in diabetes-prone biobreeding/Worcester rats is due to genetic and cell developmental defects.

Diabetes-prone BB/Wor (DP) rats lack the RT6+ peripheral T cell subset whereas diabetes-resistant BB/Wor rats have normal numbers of RT6+ T cells. Lymphocyte transfusion experiments and in vivo depletion studies have demonstrated that RT6+ T cells have an important regulatory role in the pathogenesis of insulin-dependent diabetes mellitus in BB/Wor rats. In the present study, the results of genetic complementation studies indicate that the DP rat contains an intact RT6 gene, but fails to express the RT6.1 alloantigen in the functional absence of an accessory factor (provided by RT6+ cells). At the cellular level, irradiation chimeras demonstrate that the absence of RT6+ T cells in DP rats is due to an intrinsic defect that results in abnormal development and/or differentiation of prothymocytes into RT6+ T cells. The inability of DP prothymocytes to generate RT6+ T cells is not due to serum autoantibodies, lack of accessory cells, or to the presence of inhibitory cells. Inasmuch as DP bone marrow can transfer the susceptibility for diabetes to irradiated recipients, our present results suggest that an important predisposing factor for insulin-dependent diabetes mellitus in DP rats is the inability of DP prothymocytes to generate RT6+ T cells.

Animals↗

Eradication of residual disease by administration of leukemia-specific T cells after experimental allogeneic bone marrow transplantation.

It is now well established that allogeneic lymphocytes can mediate a potent graft-vs.-leukemia (GVL) reaction when administered to bone marrow transplant (BMT) recipients. The benefit of allogeneic lymphocyte transfusion is limited because many patients develop graft-vs.-host disease (GVHD) with prolonged pancytopenia, which sometimes proves fatal. The object of the present study was to determine the antileukemic potential and GVHD risk of in vivo-generated tumor-specific allogeneic T cells given shortly after BMT. BALB/C (H-2d) mice were inoculated with different cell doses (10(5) and 5 x 10(5)) of the A20 leukemia (BALB/C origin) 2 days prior to lethal total-body irradiation (TBI) and transplantation of allogeneic, major histocompatibility complex (MHC)-matched DBA marrow grafts (H-2d, minor difference to BALB/C). Donors of BM grafts and T cells were allogeneic, MHC-matched mice (DBA, H-2d, minor difference to BALB/C). Donor-type T cells were generated from mice immunized with irradiated A20 leukemia cells or nonmalignant BALB/C splenocytes and restimulated in vitro. Whereas no significant immunotherapeutic effect was seen in mice with high tumor burden (5 x 10(5)), allogeneic BMT in mice inoculated with 1 x 10(5) A20 cells resulted in a modest antileukemic effect. This survival rate remained unchanged when 10(6) T cells obtained from donors immunized with nonmalignant BALB/C derived cells were given posttransplantation. In contrast, a single injection of 10(6) T cells from leukemia-immunized donors led to potent GVL effects without mediating clinically overt GVHD. Our data provide evidence for the hypothesis that minimal residual disease can be eradicated without inducing GVHD by administering small amounts of specific allogeneic cytotoxic T cells after BMT.

Animals↗

Salvage immunotherapy of malignant glioma.

We present the preliminary results of a phase I trial of adoptive immunotherapy for recurrent or residual malignant glioma. The protocol is based on surgical debulking followed by implantation into the tumor bed of autologous lymphocytes that have been stimulated with phytohemagglutinin-P and then cultured in vitro in the presence of interleukin 2. Fifty-five patients with a mean Karnofsky rating of 64 were treated between February 1985 and March 1987. No significant toxicity was associated with the immunotherapy. Fifty patients had a positive initial response to therapy, nine patients had early recurrence (two to four months after treatment), and 22 patients died. We comment on major differences between the protocol described and other immunotherapy protocols.

Adult↗

Management of recurrent melanoma of the extremity.

Two forms of therapy employed for treatment of patients with recurrent melanoma limited to the extremity, and carried out during different intervals of time, are presented. Perfusion of the involved extremity with phenylalanine mustard has resulted in a 5-year survival rate of 28% of 43 patients. A second group of 25 patients has been treated by a four-stage immunotherapy program consisting of sensitization with intradermal BCG, followed in 6 weeks by intra tumor injection of BCG. A third stage involved the activation of the patients's lymphocytes, after removal by a blood cell separator, incubated in vitro with irradiated neuraminidase-treated melanoma cells and reintroduced into the patient either by subcutaneous or intratumor injection. The fourth stage of immunotherapy involves injection of an inoculum of irradiated neuraminidase-treated autochothonous tumor cells plus BCG injected intratumorally or subcutaneously. Sixteen of 24 patients receiving immunotherapy treatment program have experienced arrest of their disease lasting from 5 to 42 months.

Adult↗

Immunotherapy with autologous white cell infusions ("lymphocytes") in the treatment of recurrrent glioblastoma multiforme: a preliminary report.

Autologous leukocytes (10(7) to 10(9)), obtained with the Haemonetic's Leukaphoresis apparatus, were inoculated directly into recurrent glioblastoma tumors via indwelling catheters or by direct intratumoral injection through existing craniotomy openings. The rational use for autologous leukocyte (lymphocyte) infusions was based on in vitro autologous lymphocyte cytotoxicity to glioblastoma cells in the absence of serum inhibitory factors. Seven of 17 patients treated had life expectancy under 1 month; all patients had received definitive surgery, and all but two received radiation, nitrosourea chemotherapy and/or dexamethasone, and showed evidence of clinically recurrent disease. Following autologous leukocyte infusion (lymphocyte/granulocyte ratio 1:1), eight patients sustained clinical improvement and were alive up to 17 months later. No neurotoxicity ascribable to the procedure has been observed. One patient, who was comatose at the time of single leukocyte infusion, returned to full activity and lived for 17 months without an increase in tumor mass by brain scan. These results suggest that infusions of autologous leukocytes (lymphocyte-monocytes) directly into glioblastoma may be a viable additional treatment for glioblastoma and certainly warrants further evaluation.

Adult↗

Bone marrow transplantation for severe combined immune deficiency in an infant with chimerism due to intrauterine-derived maternal lymphocytes: donor engraftment documented by chromosomal marker studies.

Chromosomal heteromorphisms defined by the quinacrine banding technique were used to identify the maternal origin of 46,XX lymphocytes present in the blood of a male infant with severe combined immune deficiency disease. These chromosomal markers were also used to document the engraftment by donor lymphocytes from the sister and the concurrent disappearance of maternal lymphocytes after a successful bone marrow transplantation. Donor lymphocytes were detected by this technique 6 days after transplantation, earlier than is usually possible with other marker systems and before definite evidence of immunoreconstitution. Maternal lymphocytes persisted in the patient's peripheral blood for a prolonged period of time, being detectable 172 days after transplantation. Analysis of T-lymphocyte- and B-lymphocyte-enriched populations after transplantation documented lymphoid chimerism with T-lymphocytes of donor origin and B-lymphocytes of both patient and donor origin, demonstrating prolonged persistence of patient B-lymphocytes and suggesting that the patient's immune defect is primarily at the T-lymphocyte level.

Bone Marrow Transplantation↗

Tridimensional study of the deep cortex of the rat lymph node. IV. Differential labelling of the deep cortex units with 3H-uridine.

Using tridimensional reconstruction, it was recently found that the deep cortex of rat lymph nodes comprises one to several basic "units." Each unit is a semi-rounded structure contiguous to the peripheral cortex and bulging into the medulla of a node. Other investigators reported that transfused lymphocytes, heavily labelled in vitro by 3H-uridine, became concentrated in an ill-defined region of nodes, referred to as the mid and deep cortex. This suggested to us that the in vivo labelling of nodes with 3H-uridine might allow to further characterize the units on a physiological basis. Therefore, rats were injected intravenously with a dose of 1--20 muCi of 3H-uridine/gm body weight and sacrificed 1 hour to 3 days later. The radioautographs of their nodes were exposed up to 535 days. The observations revealed that a large dose of 3H-uridine combined with a long exposure of the radioautographs yielded a differential labelling of the cell population of the units, characterized by a much more intense reaction than that of the surrounding structures. This demonstrated that the physiology of the lymphocyte population of the deep cortex units differs from the morphologically similar lymphocyte population of the extrafollicular zone of the peripheral cortex. The possible reason(s) for the differential labelling of the units is discussed.

Animals↗

Blood vessels of the Peyer's patch in the mouse: III. High-endothelium venules.

High-endothelium venules of mouse Peyer's patches were examined by scanning electron microscopy, and a quantitative assessment was made of the location of lymphocytes in relation to endothelial cells. Untreated mice and mice with markedly depressed levels of circulating lymphocytes were used. Lymphocytes were divided into adhering and migrating cells and as to association either with the body of the endothelial cell or with its cell border. Over 90% of all adhering cells and the great majority of migrating lymphocytes were located at the cell border. The exception was one animal in which most migrating lymphocytes appeared to penetrate the endothelial cells. Our data lend strong support to the currently held view that most migrating lymphocytes traverse the endothelium by following an intercellular path but that, under certain conditions, lymphocytes may penetrate the cytoplasm of endothelial cells.

Animals↗

Transfer of spleen cells from young to aging NZB X NZW F1 hybrid mice. Effect on mortality, antinuclear antibody, and renal disease.

Multiple injections of spleen cells from young NZB x NZW F1 hybrid mice with a mean age of 9 weeks were administered to syngeneic recipients at 10-day intervals beginning at 3 months of age. The recipient mice had a dealyed appearance of antinuclear antibody, decreased cumulative incidence of antinuclear antibody positivity up to 7.3 months of age, lower cumulative mortality up to 8 months of age, and a lesser degree of glomerular sclerosis at 8 months of age. By 9 months of age no significant differences in these parameters remained. Transferred cells were most effective during the 4- to 6-week period immediately following initiation of injections. The beneficial effects appeared to reflect an early but temporary suppression of the autoimmune process by the transferred lymphoid cells.

Aging↗

Studies on transplantation immunity. IV. Murine natural immunity to lymphoid cells in vivo.

A natural response acting to discriminate between allogeneic and syngeneic lymphocytes in vivo is described for normal mice. Eighteen to 24 h after systemic injections of low doses of 51Cr-labeled cells, less radioactivity is found in the lymph nodes after allogeneic transfer. The spleen but not the liver participates in the response. It can be abolished by neonatal induction of transplantation tolerance, is shown to be immunologically specific, and is resistant to irradiation up to 1000 rd, although a radiosensitive phase occurs during recovery from sublethal irradiation. The response is cell-mediated but depends upon cooperation from a factor present in normal serum. It is thymus-independent: this clearly distinguishes it from the superficially similar immune response acquired by immunization and aligns it with the class of responses to which the hybrid histocompatibility response and natural killer-like phenomena belong. Unlike these, however, it is present at birth and directed primarily against H-2 antigens. It appears to follow the classical transplantation rules in a limited range of strains. Some of the difficulties inherent in this type of study are discussed.

Aging↗