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PubMed1995

The role of the B cells in the adoptive transfer of collagen-induced arthritis from DBA/1 (H-2q) to SCID (H-2d) mice.

Collagen-induced arthritis (CIA) can be transferred from DBA/1 to SCID mice when native type II collagen (CII) is administered together with spleen cells, arthritis appearing some 14 days after cell transfer. In the present study, we demonstrate that both donor T- and B-lymphocyte populations play a role in this model, and that arthritis arises in SCID recipients of either murine or bovine native CII. Furthermore, the requirement for administration of soluble native CII can be replaced by subarthritogenic doses of serum from Wistar rats with CIA. In this case a fully developed arthritis appears as early as 2 days after cell transfer. However, protein G-purified IgG from CIA rat serum together with splenocytes from arthritic DBA/1 mice does not transfer arthritis. A key role of B cells in this model appears to be the production of a humoral arthritogenic factor since arthritis can be successfully transferred to SCID mice by CIA rat serum administered together with a B cell-depleted splenocyte population consisting of T cells and donor-histocompatible antigen-presenting cells. By contrast, transfer of disease cannot be achieved by co-administration of CIA rat serum and purified donor T cells, indicating that the presence of donor antigen-presenting cells is a requirement for adoptive transfer of arthritis. We propose that joint damage initiated by arthritogenic product(s) of the B cell lineage releases soluble antigens that are presented to T cells which perpetuate the disease. The finding that arthritis can be generated in SCID recipients of CIA rat serum together with splenocytes from non-arthritic DBA/1 mice immunized with denatured CII supports the hypothesis that T cells with specificity for denatured joint components perpetuate disease initiated by humoral factors.

Animals↗
PubMed1996

Adoptive transfer of resistance to murine retrovirus-induced immune suppression.

Infection of certain strains of mice, such as C57BL/6 and C57BL/10 [B10], with LP-BM5 murine leukemia virus (MuLV) rapidly causes a profound and lethal immune suppression. The H2d congenic strain of B10, B10.D2, is resistant to disease, but B10 x B10.D2 F1 mice are susceptible, indicating that disease sensitivity is dominant. To determine whether disease resistance could be adoptively transferred to a sensitive host, radiation chimeras (B10.D2 --> B10 x B10.D2 F1 and F1 --> F1) were challenged with LP-BM5 virus. Infected B10.D2 --> F1 chimeras showed no loss of immune function, whereas F1 --> F1 chimeras infected with LP-BM5 MuLV developed MAIDS and became completely immune suppressed. These results, coupled with previous studies, indicate resistance or sensitivity to disease is an inherent property of the hematopoietic system that can be transferred by bone marrow grafts.

Animals↗
PubMed1997

Augmentation of cell-mediated immunotherapy against herpes simplex virus by interleukins: comparison of in vivo effects of IL-2 and IL-7 on adoptively transferred T cells.

We investigated the ability of human recombinant interleukin-7 (IL-7) to enhance cytotoxic T lymphocyte (CTL) activity in vivo using mice infected with herpes simplex virus type-1 (HSV-1). IL-7 or interleukin-2 (IL-2) was administered twice daily to immune naive mice subjected to adoptive transfer of immune T cells after infection with HSV-1. The immunotherapeutic effect was measured by detecting the virus recovered from pinna. Administration of HSV-1 immune T cells to naive mice significantly increased their ability to clear the virus. Twice-daily injections of IL-7 at 200 IU provided an additional 20-fold reduction in virus load, compared with T cell therapy alone (P < 0.0005). Combining IL-2 and T cell therapy provided about a sevenfold reduction compared with T cell therapy alone (P < 0.0009). IL-7 also enhanced the antiviral effects of T cell therapy against HSV-1 through the enhancement of CD8+ CTLs, as observed with IL-2. These results indicate that IL-7 may be used adjunct to adoptive T lymphocyte therapy in modulating human viral diseases and cancer through enhanced immune T cell activities.

Adjuvants, Immunologic↗
PubMed1990

Adoptive transfer of viable motheaten humoral autoimmunity in cyclophosphamide-immunodepressed beige recipient mice.

Cyclophosphamide-pretreated homozygous C57BL/6 beige mice (B6 bg) were used as recipients for the transfer of lymphoid cells either of short-living autoimmune homozygous B6 'viable motheaten' mice (B6 mev) or of normal B6 mice (B6+) or B6 bg mice as controls. The grafts had no incidence on the survival of the recipients, whatever protocol used. The [mev----bg] chimeras did not develop the mev external phenotype, but there was a transfer of humoral autoimmunity. Compared to control Compared to control chimeras ([bg----bg] and [+----bg]), recipients of mev cells always showed an increase in anti-single-stranded DNA (ssDNA) antibody titres, reaching 2/3 of the mev ones 40 weeks after the cell transfers. Moreover, the anti-ssDNA were mainly of IgM class, correlating with the higher total IgM level found in [mev----bg] chimeras, thus reflecting the serological phenotype of the mev homozygous mice. Though the adoptive transfer of some mev-type humoral autoimmunity symptoms was clearly achieved in this chimera model, the recipient mice did not suffer from the several other features of the mev syndrome, such as the hyperglobulinemia and the severe pathology. This indicates that microenvironmental influences act in concert with B cells to produce pathology in mev mice.

Animals↗
PubMedDate not supplied

Experimental autoimmune damage to rat male accessory glands. II. T cell requirement in adoptive transfer of specific tissue damage.

Experimental autoimmune vesiculo-prostatitis (EAVP) was transferred within inbred Wistar rats by a relatively small number of spleen cells obtained 30 days after immunization of donors with MAG extract in CFA and injected in the internal jugular vein of recipients. Specific tissue alterations identical to those present in the glands of the donors were observed 7 days after the transfer of the cells. The main alteration present was infiltration of mononuclear cells in the interstitium accompanied by fibrosis in more severe cases and flattening of epithelium in the ventral and dorsal prostate, seminal vesicle, and occasionally in coagulating gland. Nine out of ten recipients developed sexual accessory glandular lesions of various degrees. No histological alterations were observed in the absence of cell-mediated immune response and extensive damage was only observed in rats expressing two or more positive assays. The separation of the transferred cells into enriched population of T and B cells has proved that T lymphocytes are required for the production of the tissue lesions. Depletion of T lymphocytes by nylon wool separation and anti-rat thymocytes serum and complement completely abrogate their capacity to transfer the glandular alterations. Furthermore, specific antibody precursor cells on their own seem to be incapable to promote the antibody synthesis and to initiate the glandular damage. We conclude that T lymphocytes are required for the adoptive transfer of specific tissue damage observed in autoimmune vesiculo-prostatitis as well as for the development of a cell-mediated immune response to MAG antigens. Whether the same or distinct T-cell subsets are involved in these two effects is discussed.

Animals↗
PubMedDate not supplied

New experimental model for adoptive transfer of murine autoimmune orchitis.

Previous studies demonstrated that experimental autoimmune orchitis (EAO) was produced in C3H/He mice with very high incidence by subcutaneous (s.c.) injections of viable syngeneic testicular germ cells (TC), without resorting to any adjuvants or immunopotentiators. Using this EAO model, a new and simple protocol was developed for adoptive transfer of EAO. Cell donors were C3H/He mice that received s.c. injections twice with TC alone. Spleen cells from the donors were stimulated in vitro with TC, propagated in interleukin-2 containing medium, then injected i.p. to naive recipient mice. This procedure induced severe orchitis and hypospermatogenesis with or without inflammation in epididymis and vas deferens in the recipients at high incidence. Elimination of all T cells or CD4+ T cells before the transfer produced no histopathological signs in the recipients whereas that of the CD8+ T cells or B cells had no inhibitory effect on the disease transfer, indicating that the effector cells are CD4+ T cells.

Animals↗
PubMed1994

Adoptive transfer of unresponsiveness to allogeneic skin grafts with hepatic gamma delta + T cells.

C3H/HEJ mice injected with irradiated multiple minor incompatible B10.BR lymphoid cells via the portal vein showed delayed rejection of subsequent B10.BR skin grafts. Similar delayed rejection was produced by lateral tail vein injection of B10.BR hepatic mononuclear cells or H-2k cells pulsed in vivo with B10 minor histocompatibility antigens. Inhibition of C3H anti-B10.BR immunity in vivo (assessed by delayed graft rejection) and in vitro (assessed by B10.BR-induced lymphokine production) can be transferred by radioresistant, plastic-adherent F4/80+33D1-CD4-CD8-alpha beta TcR-gamma delta TcR- mononuclear hepatic cells from (C3H/HEJ x C3H.SW)F1 mice injected 36 hr earlier with 100 x 10(6) irradiated spleen cells. By 10 days post-injection, cells transferring delayed rejection are radiosensitive, plastic non-adherent, F4/80-33D1-CD4-CD8- alpha beta Tc+- gamma delta TcR+ cells. Injection of interleukin-2 (IL-2) in vivo into mice receiving pretreatment with B10.BR cells via the portal vein, or adoptive transfer into such mice of immune anti-B10.BR lymphoid cells, abolished delayed rejection on subsequent skin grafting. Delayed rejection or modulation of lymphokine production was associated in all cases with suppression of IL-2 production and preferential retention of IL-4 production from cells stimulated in vitro.

Animals↗
PubMed1990

Adoptive transfer of autoimmune diabetes and thyroiditis to athymic rats.

We describe the induction of autoimmune diabetes, insulitis, and thyroiditis in athymic rats following injections of major histocompatibility complex compatible spleen cells. Lymphocytes with these capabilities were found in normal rats of the YOS, WAG, PVG, and diabetes-resistant BB strains, and in diabetes-prone BB rats. Adoptive transfer was facilitated by prior in vivo depletion of RT6.1+ regulatory T cells and in vitro mitogen activation of donor spleen cells. By RT6 depleting diabetes-resistant donors and using nude recipients, transfer of diabetes and thyroiditis was accomplished by using fresh, unstimulated spleen cells. The data suggest that organ-specific autoreactive cells may be present to various degrees but suppressed to a variable extent in many rat strains. The equilibrium between autoreactive and regulatory cells appears to determine the expression of autoimmunity.

Animals↗
PubMed1994

Adoptive transfer of polyclonal and cloned cytolytic T lymphocytes (CTL) specific for mouse AIDS-associated tumors is effective in preserving CTL responses: a measure of protection against LP-BM5 retrovirus-induced immunodeficiency.

Cytolytic T lymphocytes (CTL) can be raised against C57BL/6 B-cell lymphomas from mice with LP-BM5 murine leukemia virus-induced AIDS (MAIDS). Adoptive transfer of polyclonal anti-MAIDS tumor CTL or two CTL clones specific for the B6-1710 MAIDS lymphoma caused preservation of major histocompatibility complex-restricted and allogeneic CTL responses, which may be interpreted as indices of protection from LP-BM5 murine leukemia virus-induced immunodeficiency.

Animals↗
PubMed1993

Magnetic resonance imaging investigation of blood-brain barrier damage in adoptive transfer experimental autoimmune encephalomyelitis.

Recent advances in fast magnetic resonance imaging (MRI) techniques have allowed quantification of parameters such as T1 relaxation time, which can be modified by changes in the water content of a tissue. We have used this new method to study the evolution of blood-brain barrier (BBB) changes after adoptive transfer of MBP-specific (AT-EAE) and ovalbumin-specific T cell lines in Lewis rats. Measurable changes in T1 relaxation time suggesting widespread increase in BBB permeability were found, starting on day 3 post inoculation (p.i.), in the midbrain and brainstem of AT-EAE rats. In addition, we noted a significant decrease in T1 relaxation time before injection of a paramagnetic agent, in the cisternal cerebrospinal fluid (CSF) of diseased animals, starting on day 5 p.i. In vitro measurement of T1 in CSF containing various concentrations of albumin, IgM and glucose showed that, at physiological concentrations, a T1 decrease is mainly associated with an increase in albumin concentration. A moderate increase in BBB and blood-CSF barrier permeability was found as early as 4-8 h p.i., in rats injected with MBP-specific as in animals injected with ovalbumin-specific T cell lines, suggesting a non-specific mechanism. Experimental MRI may become a powerful tool to sequentially analyse changes in barrier dynamics, for example following pharmacological intervention.

Animals↗
PubMedDate not supplied

Biologic effects of the adoptive transfer of cells depleted of monocytes with L-phenylalanine methyl ester.

Monocytes macrophages have negative regulatory effects on many immunologic responses. Depletion of monocytes from peripheral blood using the lysosomotropic agent, L-phenylalanine methyl ester (PME), has been shown to improve lymphokine activated killer (LAK) cell expansion in vitro. A pilot study of the adoptive transfer of LAK cells expanded with PME was performed in patients with metastatic renal cell carcinoma. Patients received interleukin-2 (IL-2) by continuous infusion for 5 days. Leukopheresis was performed daily for 4 days during the second week. Cells obtained from 8 patients were depleted of monocytes using PME in an one-step procedure; < or = 3% of the remaining cells were monocytes. All cells were expanded for 10 days in air-porous plastic bags with IL-2. Cells expanded 2.7-fold when depleted with PME and 1.7-fold when not depleted (P = 0.02). Expanded cells were administered together with IL-2. Patients received up to 60 x 10(10) PME-depleted cells (mean = 26 x 10(10)) with LAK activity (% lysis) of 60 +/- 12%. Lymphocyte phenotype and cytolytic activity were not modulated by PME-depletion, and clinical toxicities and systemic immunologic effects observed in patients receiving PME-depleted cells were similar to that of 5 patients receiving cells not expanded with PME. Thus, the use of PME to deplete monocytes ex vivo can result in the yield of large number of effectors that retain immunologic activity for potential clinical use. The process is convenient, efficient, and does not add clinical toxicity.

Carcinoma, Renal Cell↗
PubMed2000

Development, characterization and distribution of adoptively transferred peripheral blood lymphocytes primed by human papillomavirus 18 E7--pulsed autologous dendritic cells in a patient with metastatic adenocarcinoma of the uterine cervix.

We describe a 27-year-old woman with systemic chemoresistant and radioresistant metastatic disease secondary to a recurrence of human papillomavirus (HPV) 18 infected cervical adenocarcinoma of the uterine cervix who received adoptive transfer of peripheral blood T cells stimulated with HPV 18 E7-pulsed autologous dendritic cells (DC). Extensive in vitro characterization of the DC-activated T cells derived from peripheral blood mononuclear cells (PBMC) included phenotypic analysis, cytotoxicity and intracellular cytokine production. High cytotoxicity activity was observed by CD8+T cells against autologous tumor cells, but not against NK-sensitive K562 cells, autologous Con-A lymphoblasts, or autologous Epstein-Barr virus-transformed lymphoblastoid cells. Blocking studies demonstrated that lytic activity was significantly inhibited by pretreatment of tumor targets with MAb specific for HLA class I as well as that of effector cells with anti-CD8, anti-LFA-1, but not anti CD3 MAb. Two-color flow cytometric analysis of the cytotoxic T cells revealed that a significant proportion of CD8+ cells was also CD56+. These double positive CTLs were thymically derived, as shown by expression of heterodimeric CD8 molecules (alpha/beta CD8) and were endowed with high cytotoxic activity against tumor cells. Analysis of intracellular cytokine expression showed that the striking majority of E7-pulsed DC activated CD8+ T cells strongly expressed IFN-gamma, TNF-alpha and IL-2 but not IL-4. The patient received two infusions of cytotoxic tumor-specific T cells at 2 week intervals, and in vivo distribution of the T cells was followed by 111 oxine labeling and serial gamma camera imaging. Persistent accumulation of radioactivity in the lungs, which harbored extensive metastatic disease, was detected up to 120 hrs after the infusion. Taken together, these results illustrate the potential of E7-specific and tumor-specific CTL-based immunotherapy for the treatment of patients with invasive cervical cancer.

Adenocarcinoma↗
PubMed1994

Adoptive transfer of protection to Taenia taeniaeformis infection in rats with immune spleen cells.

The effector mechanism of the protection against re-infection with eggs of Taenia taeniaeformis was evaluated in rats by analysing protection dynamics against an ongoing primary infection. Immune spleen cells were prepared from F344 donor rats 10 days after oral inoculation with 200 eggs and used for adoptive transfer experiments. When F344 recipient rats were injected intravenously with immune spleen cells (2 x 10(8)) from 2 to 48 h after a primary egg inoculation, there was a statistically significant reduction in the number of metacestodes recovered at day 30 of the infection. The highest protection figures were obtained in rats given immune cells at 12 or 24 h of the primary infection. The maximum reduction induced with immune cells was 92% when they were injected at 12 h of the ongoing infection. It is strongly suggested that the vulnerable stage of the parasite damaged by immune spleen cells is the initial stage of infection (oncosphere and post-oncosphere stages in the liver within 2 days, especially between 12 and 24 h).

Animals↗
PubMed2000

Adoptive transfer of human natural killer cells in mice with severe combined immunodeficiency inhibits growth of Hsp70-expressing tumors.

In vitro, tumor-selective Hsp70 plasma membrane localization correlates with increased sensitivity to lysis mediated by a subpopulation of human natural killer (NK) cells that adhere to plastic following cytokine stimulation. In the present study, we analyzed the capacity of adoptively transferred human NK cells in SCID/beige mice for local tumor control and prevention of metastatic dissemination of Hsp70-expressing CX(+) and non-expressing CX(-) tumors following orthotopic (o.t.) injection. Both tumor sublines were derived by cell sorting of the original cell line, CX2, and thus exhibit an identical MHC and adhesion molecule expression pattern but differ with respect to Hsp70 plasma membrane expression. Viability of adherent, human NK cells in SCID/beige mice up to 18 days and the capacity to migrate have been demonstrated. Growth of Hsp70-expressing and non-expressing CX(+) and CX(-) tumor cells was completely suppressed when 10 x 10(6) NK cells were injected into the i.p. cavity on day 4 after inoculation of 2.5 x 10(6) tumor cells. Although a single injection of 5 or 2.5 x 10(6) NK cells was not sufficient to suppress tumor growth completely in all mice, the reduction in size of CX(+) tumors was significantly greater than that of CX(-) tumors. To mimic the clinical situation, ex vivo stimulated NK cells were injected i.v. on day 4 after o.t. injection of tumor cells. Under these conditions, growth of Hsp70-expressing primary tumors and metastases was suppressed. If CX(-) tumor cells were injected, 3 of 9 mice developed Hsp70-negative primary tumors. However, none of these mice developed distant metastases. In summary, our data indicate that Hsp70 acts as a recognition structure for adherent NK cells in a SCID/beige mouse model.

Animals↗
PubMed1985

Adoptive transfer of murine relapsing experimental allergic encephalomyelitis.

Relapsing experimental allergic encephalomyelitis (EAE), an autoimmune disorder resembling multiple sclerosis, has been produced by inoculating SJL/J mice with spinal cord or myelin basic protein in appropriate adjuvants. To determine whether initially sensitized lymphocytes or the persistence of antigen depots in the animal were responsible for the relapsing episodes of inflammatory demyelination, adoptive transfer studies were undertaken utilizing lymphocytes from relapsing EAE-immunized donors transferred directly or after in vitro culture. In direct-transfer studies donor lymphocytes produced clinical and pathological signs of relapsing EAE in 3 of 7 recipients of lymph node lymphocytes and 1 of 5 recipients of splenic lymphocytes. In vitro culture of lymphocytes in myelin basic protein or T cell growth factor prior to transfer increased both the incidence of disease and the number of animals having relapses, and allowed transfer with fewer lymphocytes. Because all animals had delayed onset of disease, this study demonstrates that the ability to develop relapsing inflammatory demyelination is transferable with lymphocytes and does not require the presence of antigen.

Animals↗
PubMed1978

Plasmodium chabaudi in mice. Adoptive transfer of immunity with enriched populations of spleen T and B lymphocytes.

Thymectomized NIH and C57BL mice were more susceptible to Plasmodium chabaudi than controls, indicating a role for T cells in acquired immunity to the parasite. Enriched populations of T and B cells were prepared from the spleens of immune mice using nylon-wool columns, and were adoptively transferred to syngeneic non-irradiated mice or mice irradiated with 600 or 800 rad. Some immunity could usually be transferred with immune T, B and glass-wool (g.w.) filtered spleen cell populations. In the heavily irradiated mice g.w. filtered immune spleen cells gave the best protection and the immune T cells the least. Preliminary attempts to show synergistic activity between immune T and B cells in irradiated mice were not successful.

Animals↗
PubMed1985

Adoptive transfer of small bowel intraepithelial and Peyer's patch lymphocytes from orally immunised animals: effects on the antibody response to parenteral antigen.

Intraepithelial (IEL) and Peyer's patch lymphocytes (PPL) were isolated from the small bowel mucosa of mice in which specific systemic antibody responses to ovalbumin (OVA) had been suppressed by oral exposure to that antigen. These lymphocytes were then adoptively transferred into syngeneic animals. The PPL transferred 24 h after oral OVA showed a tendency to depress secondary serum antibody responses to intraperitoneal OVA in the recipients. Conversely, IEL transferred 1-5 days after oral OVA significantly enhanced specific serum antibody responses.

Animals↗
PubMed1986

T-cell immunity in murine malaria: adoptive transfer of resistance to Plasmodium chabaudi adami in nude mice with splenic T cells.

Acute infections caused by the murine malarial parasite Plasmodium chabaudi adami are resolved by antibody-independent mechanisms of immunity. The fact that athymic nude mice developed high-grade unrelenting malaria and died when infected with this parasite suggested a significant role for T lymphocytes. Using adoptive transfer techniques, we demonstrated that spleen cells from either nonimmune or immune donor BALB/c mice eventually suppressed P. chabaudi adami infections in histocompatible recipient nude mice in a dose-dependent manner. Infections in recipients of "immune" spleen cells were less severe, demonstrating a depressed peak parasitemia and a shortened duration of patent infection, than was observed in recipients of normal spleen cells. Also, when sufficient numbers of immune spleen cells were transferred, the second wave of parasitemia (characteristic of this infection in nonimmune mice) failed to occur. T lymphocytes mediated protection in recipient mice, since T-cell-enriched, but not B-cell-enriched, spleen cell fractions suppressed P. chabaudi adami infections in nude mice. Protection was best achieved with T cells that bore the L3T4 phenotype. Patent parasitemias developed in all recipient mice, suggesting that the grafted cells did not limit parasite growth directly but achieved this end by activating other as yet unidentified inhibiting cell systems.

Animals↗