Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Adoptive Transfer”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 505 records · Page 28Linked to original sources
PubMed1990

Adoptive transfer of diabetes in BB rats induced by CD4 T lymphocytes.

Unseparated splenocytes (SPCs) or purified SPC subsets from diabetes-prone BB (BBdp) or diabetic BB (BBd) rats were activated in vitro with either phorbol myristate acetate (PMA) and ionomycin (I) or concanavalin A (ConA). Such activated SPCs were then injected intravenously into 30-day-old BBdp rats, and their capacity to induce adoptive transfer (AT) of diabetes was studied. The proliferative response in vitro of BBd unseparated SPCs or purified W3/13+ SPCs (i.e., T lymphocytes + large granular lymphocytes) to PMA + I far exceeded that of ConA, resulting in mean stimulation indices of 68 and 112 (PMA + I) and 1.9 and 30 (ConA). The incidence of AT was similar when equal numbers of unseparated SPCs from the same BBd donor were injected after activation by either PMA + I + interleukin 2 (PII) or ConA (57 vs. 50%, respectively); however, injection of PII-activated and macrophage-depleted W3/13+ SPCs from BBd animals resulted in a significantly higher incidence of AT (90%, P less than 0.05). As few as 0.5 x 10(6) PII-activated W3/13+ SPCs were sufficient to induce AT. Sixteen percent of recipients developed diabetes after injection of activated W3/13+ cells from 40-day-old BBdp donors. To determine which W3/13+ cells might mediate such transfer, purified and PII-preactivated CD4 T lymphocytes from BBd rats were injected, and they succeeded in AT in 44% of the recipients. Preactivated BBd B lymphocytes were unable to induce AT. Although a possible role for large granular lymphocytes cannot be excluded, the results demonstrate that in the BB rat, the beta-cell destruction can be induced by CD4 T lymphocytes.

Animals↗
PubMed1991

Effect of adoptive transfer of cloned Actinobacillus actinomycetemcomitans-specific T helper cells on periodontal disease.

Previously we isolated several Actinobacillus actinomycetemcomitans-specific T-cell clones from the spleens and lymph nodes of immunized Rowett rats. These clones were characterized as W3/13+, W3/25+, OX8-, and OX22-, suggesting a T helper (Th) phenotype. In the current experiments, 10(6) cells from a single A. actinomycetemcomitans-specific clone (A3) were adoptively transferred to a group (AaTh; n = 13) of normal heterozygous rats (rnu/+) at 28 days of age. A second group received no T cells (AaNT; n = 15), and a third group also received no T cells (NAaNT, n = 11). Beginning 1 day after transfer, the first and second groups were infected orally with A. actinomycetemcomitans for 5 consecutive days. The presence of infection was confirmed immediately after challenge and after 5 months, when the experiments were ended. Significantly higher numbers of lymphocytes were recovered from the gingival tissues of the first group than from those of either of the other groups. Also, this group showed significantly elevated (P less than 0.01) serum immunoglobulin G and immunoglobulin M antibody to A. actinomycetemcomitans in an enzyme-linked immunosorbent assay when compared with both other groups. Bone loss was significantly lower (P less than 0.01) in recipients of A. actinomycetemcomitans-specific cloned cells when compared with the other infected group and was approximately equal to the bone loss of the uninfected group. These results are consistent with the hypothesis that T-cell regulation can affect periodontal disease. In this regulation, T helper cells appear to interfere with periodontal bone loss.

Actinobacillus↗
PubMed2001

Antitumor immunity induced by laser immunotherapy and its adoptive transfer.

The ideal cancer treatment modality should not only cause tumor regression and eradication but also induce a systemic antitumor immunity, which is essential for control of metastatic tumors and for long-term tumor resistance. Laser immunotherapy using a laser, a laser-absorbing dye, and an immunoadjuvant has induced such long-term immunity in treatment of a mammary metastatic tumor. The successfully treated rats established total resistance to multiple subsequent tumor challenges. To further study the mechanisms of the antitumor immunity induced by this novel treatment modality, passive adoptive transfer was performed using splenocytes as immune cells. The spleen cells that were harvested from successfully treated tumor-bearing rats provided 100% immunity in the naive recipients. The passively protected first cohort rats were immune to tumor challenge with an increased tumor dose; their splenocytes also prevented the establishment of tumor in the second cohort of naive recipient rats. This immunity transfer was accomplished without the usually required T-cell suppression in recipients.

Animals↗
PubMed1985

Interferon in experimental autoimmune encephalomyelitis (EAE): effects of exogeneous interferon on the antigen-enhanced adoptive transfer of EAE.

The transfer of experimental autoimmune encephalomyelitis (EAE) can be enhanced by incubating lymph node cells (LNC) from EAE rats with myelin basic protein (MBP). Addition of rat fibroblast interferon (RfIFN) to cultures of EAE-LNC just before the addition of MBP, resulted in the inhibition of the adoptive transfer of EAE. Both development of clinical signs, such as weight loss and hind limb paralysis, and histopathological lesions, lymphocytic perivascular infiltrates of the central nervous system, were inhibited by the addition of RfIFN to a final concentration of 300 U/ml or higher. This inhibition was dose dependent and appeared to be mediated primarily by the antiproliferative action of RfIFN.

Animals↗
PubMed1991

rIL-1 alpha enhances adoptive transfer of resistance to Listeria monocytogenes infection.

We have previously demonstrated that administration of recombinant rIL-1 alpha enhances resistance against Listeria monocytogenes infection in mice. In this study we considered the possibility that this cytokine might also augment adoptive immunity conferred by the transfer of listeria-immune spleen cells. Concomitant administration of rIL-1 alpha with large numbers (2 x 10(7) or 10(8)) of listeria-immune spleen cells reduced the protection mediated by the transferred cells. Conversely, rIL-1 alpha co-administered with suboptimal numbers (1-5 x 10(6)) of immune splenocytes augmented anti-listeria resistance in an additive fashion. Although transfer of 10(6) listeria-immune spleen cells alone did not result in significant protection, when 10(6) immune cells were incubated with rIL-1 alpha prior to transfer they conferred significant protection to naive recipients. Time course experiments indicated that the greatest protection was achieved when listeria-immune spleen cells were pretreated with rIL-1 alpha for 2 h prior to adoptive transfer. The protection transferred by 10(6) rIL-1 alpha-pretreated immune spleen cells was not inhibited by TGF beta. This study is the first to use rIL-1 alpha to potentiate the adoptive transfer of resistance to an infectious agent by immune cells.

Animals↗
PubMed1987

Fate of gamma-interferon-activated killer blood monocytes adoptively transferred into the abdominal cavity of patients with peritoneal carcinomatosis.

Five patients with colorectal cancer widely metastatic to peritoneal surfaces have been treated i.p. with infusions of autologous blood monocytes made cytotoxic by in vitro incubation with human gamma-interferon. The monocytes were purified by a combination of cytapheresis and counter-current centrifugal elutriation procedures; each week approximately 350 million activated monocytes were given to patients as adoptive immunotherapy by a single i.p. instillation. On the eighth cycle of treatment the trafficking of i.p. infused blood monocytes was studied in two patients by prelabeling the cells with 111In. These activated cells became distributed widely within the peritoneal cavity. Two and 5 days after infusion their position within the peritoneum had not changed. When peritoneal specimens were obtained 36 h after 111In-labeled monocyte infusion, labeled monocytes were demonstrated to be associated with the serosal surfaces by autoradiographic analysis. Scintiscanning structures outside the abdominal cavity revealed that 111In-labeled monocytes infused i.p. did not traffic to other organs during the 5 days of the study. We conclude that i.p. adoptive transfer of autologous killer blood monocytes is an effective way of delivering these cytotoxic cells to sites of tumor burden on peritoneal surfaces in these cancer patients.

Colonic Neoplasms↗
PubMedDate not supplied

Immunotherapy of murine sarcoma by adoptive transfer of resident peritoneal macrophages proliferating in culture.

Normal resident peritoneal macrophages from BALB/c mice were continuously grown and expanded in vitro as non tumorigenic cells on a confluent layer of mesothelial cells. These peritoneal macrophages expanded in vitro (EPM) were very cytotoxic against EMT6 sarcoma, Abelson myeloma, EL4, and L929S cells in culture. This tumoricidal effect was fully expressed without further activation with bacterial lipopolysaccharides (LPS). In vivo, adoptive transfer of one million EPM to BALB/c mice bearing subcutaneous EMT6 sarcoma caused regression of the solid tumor. In contrast, macrophages produced by 10 days' culture of bone marrow stem cells, or freshly isolated from the peritoneal cavity of BALB/c mice, were not cytotoxic in vitro or in vivo. Local injection in the vicinity of the tumor as well as intravenous transplantation of EPM effectively inhibited tumor growth. This antitumoral effect was further enhanced by intraperitoneal injection of 2 micrograms LPS to the tumor bearing mice.

Animals↗
PubMed1982

Thymus dependence of the adoptive transfer of intestinal mastocytopoiesis in Trichinella spiralis-infected mice.

The relationship between the gut and mesenteric lymph node in the kinetics of mucosal mast cells (MMC) was further analysed. A Trichinella-induced synchronous proliferation of MMC occurred in the intestine of thymus-bearing and not in athymic mice, both at sites of parasite invasion (jejunum) and elsewhere (caecum) and in the mesenteric lymph node. The mastocytopoietic ability could be adoptively transferred with immune mesenteric lymph node cells to the jejunum and caecum of infected thymus-bearing recipients. The enhanced mastocytopoiesis which was both antigen- and thymus-dependent, was only observed for the stroma intestinal mast cells (IMC) and not for the intraepithelially located globule leucocytes (GL). The data suggest a common source for IMC in intestinal mucosae and support the idea that IMC and GL are two independent cell populations.

Animals↗
PubMed1995

Antibody responses to allergen Lol pIV are suppressed following adoptive transfer of B lymphocytes from the internal image anti-idiotypic antibody-treated mice.

An internal image anti-idiotypic antibody, designated B1/1, was generated against an idiotope (Id91) of the monoclonal antibody (mAb91) specific for Lol pIV. The administration of B1/1 in PBS, at doses ranging from 100 ng to 100 micrograms/mouse, to syngeneic Balb/c mice resulted in the suppression of the formation of anti-Lol pIV antibodies that possessed the Id91. Spleen cells obtained from the mice 2 weeks after the treatment with B1/1 (25 micrograms/mouse) were adoptively transferred intravenously into the syngeneic recipients which were challenged intraperitoneally with Lol pIV in alum 2 hr after the transfer. The recipients were boosted with Lol pIV 14 days later. It was demonstrated that the transfer of splenic B cells (but not of T cells) from B1/1-treated donors induced a significant suppression of not only the level of IgE and IgG antibodies to Lol pIV, but also the level of antibodies possessing the Id91. Treatment of the B cells with mAb91 plus complement abrogated their ability to transfer the suppression. This study indicates that the treatment with the anti-Id B1/1 generated B cells that were characterized, serologically, as possessing the anti-Id-like antibodies on their surface and were responsible for transferring the suppression of the formation of antibodies to allergen Lol pIV and the expression of Id91.

Allergens↗
PubMed1985

Adoptive transfer of anti-syphilis immunity with lymphocytes from Treponema pallidum-infected guinea pigs.

Spleen and lymph node cells taken from strain 2 and strain 13 guinea pigs at the peak of their primary immune response to cutaneous syphilitic infection could transfer partial protection to symptomatic disease to normal syngeneic recipients challenged with the Nichols strain of Treponema pallidum. These recipients of immune cells had significantly fewer treponemes disseminating to the regional lymph nodes and developed fewer and less severe cutaneous lesions that resolved faster than those in guinea pigs that had been infused with normal lymphoid cells. Immune donor cells also had the capacity to transfer specific delayed-type hypersensitivity responses for T. pallidum antigens. Both T and B cells were effective in conferring anti-syphilis immunity which was associated with the almost immediate development and persistence of substantially elevated levels of circulating anti-treponemal antibody in the protected recipients. Our findings in this adoptive transfer system provide the first direct experimental evidence implicating both cellular and humoral components of the immune response as important effector mechanisms in host resistance to the pathogenic spirochete causing venereal syphilis.

Animals↗
PubMed1984

Depressed in vitro and in vivo antibody response and adoptive transfer of delayed hypersensitivity to myoglobin with spleen cells of mice chronically infected with Schistosoma japonicum and injected with myoglobin.

Spleen cells from C57BL/6J mice infected for 21 weeks with Schistosoma japonicum did not show an in vitro secondary antibody response upon challenge with sperm whale myoglobin. Mice infected for 13 weeks showed almost no in vivo secondary antibody response to this antigen. Spleen cells from mice infected for 12 to 21 weeks did not adoptively transfer delayed hypersensitivity to this antigen.

Animals↗
PubMed1996

Immunological and metabolic effects of prophylactic insulin therapy in the NOD-scid/scid adoptive transfer model of IDDM.

Prophylactic insulin therapy prevents IDDM in spontaneous animal models of the disease and has shown promise in preventing the disease in humans. Although large clinical trials have been formed to use this therapy, a comparative analysis of the efficiency of different pharmaceutical forms and doses of insulin in preventing IDDM has not been performed, and the mechanism underlying the observed prevention of disease is unknown. In the NOD-scid/scid adoptive transfer model of IDDM (10(7) new-onset NOD splenocytes injected intravenously into 6- to 8-week NOD/scid-scid recipients; insulitis develops at 6-9 days post-transfer and 100% IDDM by 32 days post-transfer), life-table (log-rank) analyses revealed that IDDM can be delayed (compared with insulin-free diluent, once daily, n = 8) with equivalent efficiency by prophylactic administration (-9-50 days post-transfer) of high (metabolism-altering) doses of short-acting (0.5 U, once daily, regular, n = 13) or long-acting (0.5 U, once daily, ultralente, n = 9) insulin as well as non-metabolism-altering low-dose insulin (0.02 U, once daily, regular, n = 8). Furthermore, IDDM was delayed with somatostatin (0.2 microgram, twice daily, n = 11), an agent that suppresses endogenous insulin production. No significant difference was seen between the preventative effects of these agents. In an assessment of when therapies can be initiated and still maintain clinical efficiency, only prophylactic somatostatin therapy delayed IDDM (n = 10, P = 0.02) when initiated at 14 days post-transfer, whereas the short-acting insulin regimen did not retard the onset of IDDM (n = 8, P = 0.25) compared with diluent-treated controls. The 24-h urinary C-peptide levels were significantly reduced with short-acting (-56%, P = 0.01) and long-acting (-67%, P = 0.02) insulin products and somatostatin (-59%, P = 0.02) compared with diluent-treated controls. These results indicate that both immunological and metabolic (i.e., beta-cell rest) factors may contribute to the beneficial effects of prophylactic insulin therapy.

Animals↗
PubMed1982

Failure of serum from recovered rats to prevent enhanced adoptive transfer of experimental allergic encephalomyelitis.

The rat is unique among species used for research on experimental allergic encephalomyelitis (EAE) because of the spontaneous recovery which occurs routinely after severe, almost fatal disease. The mechanism of recovery has never been adequately explained although it has been suggested that suppressor cells might play a role in this phenomenon. In another immune system (contact sensitivity) anti-idiotypic antibodies obtained during the recovery phase have been shown to have a protective effect. Adoptive transfer of EAE, which can be markedly enhanced by incubation of sensitized cells with antigen in vitro, offers a convenient tool for investigating mechanisms of recovery. With this system, we have attempted to suppress transfer of disease with serum obtained from recovered rats. In spite of various manipulations of the experimental protocol, including the use of serum plus complement before and after incubation of cells with antigen, we have been unable to demonstrate suppression of disease. We and others recently reported that cells from recovered rats are also capable of enhanced transfer. This permitted the use of autologous serum from individual cell donors. Even in this strictly autologous system, however, no inhibitory effect of serum could be detected.

Animals↗
PubMed2002

Indoleamine 2,3-dioxygenase expression in transplanted NOD Islets prolongs graft survival after adoptive transfer of diabetogenic splenocytes.

Indoleamine 2,3-dioxygenase (IDO) catalyzes the breakdown of the amino acid tryptophan into kyneurenine. It has been shown that IDO production by placental trophoblasts prevents the attack of maternal T-cells activated in response to the paternal HLA alleles expressed by the tissues of the fetus. In this article, we show that adenoviral gene transfer of IDO to pancreatic islets can sufficiently deplete culture media of tryptophan and consequently inhibit the proliferation of T-cells in vitro. Experiments in vivo have also demonstrated that transplantation of IDO-expressing islets from prediabetic NOD mouse donors into NODscid recipient mice is associated with a prolongation in islet graft survival after adoptive transfer of NOD diabetogenic T-cells. This protection is attributed to the depletion of tryptophan at the transplantation site beneath the kidney capsule. These results suggest that local modulation of tryptophan catabolism may be a means of facilitating islet transplantation as a therapy for type 1 diabetes.

Adenoviridae↗
PubMed1989

Modulation of acute and latent herpes simplex virus infection in C57BL/6 mice by adoptive transfer of immune lymphocytes with cytolytic activity.

The ability of highly lytic herpes simplex virus (HSV) cytolytic T lymphocytes to modulate the interaction between the murine host (adult C57BL/6 [H-2b] mice) and HSV type 1 Patton resulting in acute infection in the footpad and latent infection in the sensory lumbosacral dorsal root ganglia (L6, L5, L4, and L3) innervating the footpad was investigated. Results indicated that a critical threshold level of infectious HSV was required to establish infection. The adoptive transfer of cytolytic T lymphocytes derived from in vitro cultures after restimulation with HSV-infected, syngeneic stimulator cells exhibiting class I H-2-restricted, L3T4- Lyt-2+ HSV-specific cytolytic activity immediately before infection with a high dose of HSV reduced the levels of infectious HSV recovered from the footpad tissue during acute infection and the levels of latent HSV reactivated from the dorsal root ganglia to levels expected from mice infected with a low dose. Depletion of Lyt-2+ cells from the transferred population abrogated the protective ability, while depletion of L3T4+ cells had little effect. These results suggest that functionally lytic HSV-specific cytolytic T lymphocytes present at the time of HSV infection have the potential to participate in the control of the acute infection and in the subsequent establishment of latent infection.

Animals↗
PubMed1981

Alteration of clonal profile. III. T15 ontogenetic advantages are not sufficient for establishing idiotypic dominance in adoptive transfer.

We have examined the ontogeny of BALB/c plaque-forming cell (PFC) responses to phosphorylcholine (PC) from fetal and neonatal liver by using the (CBA/N x BALB/c)F1 transplantation model. In this system, thymus-dependent (PC-keyhole limpet hemocyanin) and thymus-independent class 1 (PC-Brucella abortus, PC-lipopolysaccharide) PC antigens stimulate B cell subpopulations, which functionally emerge early after transfer. Responsiveness to a thymus-independent class 2 antigen, C-polysaccharide extract of a Streptococcus pneumoniae mutant, is acquired later. The response to PC antigens tested initially exhibited T15 dominance. Non-T15 clones, which are not expressed to a great degree in normal BALB/c mice, are inherently slow in their rate of maturation; in adoptive transfer, however, they eventually comprise much of the transplanted anti-PC PFC response. Obviously, the advantages the T15 subset has in ontogeny do not result in idiotypic dominance once the immature cells are removed from the intact BALB/c environment. We discuss possible regulatory mechanisms involved in the alteration of the T15+:T15- ratio.

Animals↗
PubMedDate not supplied

Tumor blood supply and tumor localization by adoptively transferred IL-2 activated natural killer cells.

The circulatory pattern of IL-2 activated natural killer (A-NK) cells was studied in C57BL/6 mice bearing 10 day-old pulmonary and subcutaneous (s.c.) metastases of the B16 melanoma in order to evaluate the roles of the concentration of A-NK cells in the blood and of tumor blood flow on accumulation of A-NK cells in tumors. Kinetic studies of the presence of A-NK cells in peripheral blood after adoptive transfer revealed that these cells rapidly disappear from the blood. Via intravital microscopy of animals with exposed lung tissue, we have shown that the vast majority of transferred A-NK cells become efficiently arrested within the lung microcirculation at their first encounter with this organ, thereby explaining the fast disappearance of the cells from the bloodstream. Despite the low number of A-NK cells circulating in the blood, systemically injected A-NK cells (20 million per mouse) localized significantly (70-80 million cells/g) into most pulmonary metastases within 8-16 hours. In contrast, very few A-NK cells (< 0.2 million cells/g) were found in the s.c. metastases. Based on measurements of tumor blood flow (showing a classic inverse relationship between tumor size and tumor blood flow) and the blood concentration of A-NK cells, we estimated the highest intratumoral density of A-NK cells that theoretically can be generated by A-NK cells transported to the tumor by way of the blood. In s.c. tumors, the observed density of A-NK cells was at all times lower (10-50 fold) than the estimated density, indicating that only a few percent of the A-NK cells arriving at these tumors become retained in them. In contrast, the observed density of A-NK cells in pulmonary metastases was at all times higher (2-3 fold) than the estimated density. This finding indicates that A-NK cells might not reach the pulmonary metastases solely by way of the blood stream. In conclusion, i.v. injected A-NK cells become immediately entrapped in the lungs and, consequently, circulate poorly. While lung metastases become significantly infiltrated by i.v. injected A-NK cells, metastases in organs down-stream from the lungs become poorly infiltrated. We hypothesize that only a part of the A-NK cells found in lung metastases 8-16 hours following injection reach these metastases by way of the blood-vascular system. They might also migrate into the metastases from the surrounding normal lung tissue.

Animals↗
PubMed1981

Recovery of mice from herpes simplex virus type 2 hepatitis: adoptive transfer of recovery with immune spleen cells.

Young BALB/c mice inoculated intraperitoneally with herpes simplex virus type 2 develop focal necrotizing hepatitis. After infection, the livers of these mice show increasing virus titers, which reach a maximum on day 3 after infection; this is followed by a dramatic decrease in the amount of virus recovered on days 4 and 5. This decrease in virus content is accompanied by a progressive infiltration of the lesions with mononuclear leukocytes and an apparent resolution of the lesions. Adoptive transfer of immune spleen cells from mice infected 6 days earlier accelerated this process. When 50 x 10(6) to 100 x 10(6) immune spleen cells were transferred 24 h after infection, the inflammatory response and the clearance of virus from the livers were advanced by almost 2 days. As few as 12 x 10(6) immune spleen cells accelerated the healing process, whereas fewer immune cells, disrupted immune cells, or normal spleen cells did not have an effect. The protection conferred by herpes simplex virus type 2-sensitized immune spleen cells was specific since mouse cytomegalovirus- or vaccinia virus-sensitized immune spleen cells had no effect on the course of infection with herpes simplex virus type 2, whereas some cross-reactivity was observed between herpes simplex virus types 1 and 2. This model seems to be suitable for examining the immunological mechanisms that are active during recovery from visceral herpes simplex virus infections.

Animals↗