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PubMed1993

Adoptive transfer of experimental allergic neuritis in the immune suppressed host.

Experimental allergic neuritis (EAN) was induced in normal and irradiated Lewis rats by passively transferring T cells sensitized to SP-26, a peptide fragment of P2 myelin protein. The recipients became sick 4-8 days post transfer and the degree of disability correlated directly with the dose of T cells. Smaller doses caused demyelination of nerve roots and sciatic nerves and larger doses produced more severe demyelination and significant axonal degeneration. Irradiated recipients developed similar clinical EAN and showed macrophage-mediated demyelination despite severe suppression of the host inflammatory response.

Animals↗
PubMed1996

Adoptively transferred CD8+ T lymphocytes provide protection against TMEV-induced demyelinating disease in BALB/c mice.

On intracerebral infection with the BeAn strain of Theiler's murine encephalomyelitis virus (TMEV), certain mouse strains develop a chronic demyelinating disease similar both clinically and pathologically to human multiple sclerosis. Other strains remain resistant. We previously established that differential susceptibility to this demyelinating disease exists among BALB/c substrains, with BALB/cAnNCr mice being susceptible while BALB/cByJ mice are resistant. BALB/cByJ mice are rendered susceptible to TMEV-induced demyelination on exposure to low dose gamma-irradiation before TMEV infection. BALB/cAnNCr and irradiated, infected BALB/cByJ animals are protected against TMEV-induced demyelination by the transfer of a splenic population from TMEV-infected BALB/cByJ donors. Resistance to demyelination appears to be mediated by a CD8+ radiosensitive population, which is induced on infection with TMEV and which must act early to establish resistance to TMEV-induced demyelination.

Animals↗
PubMed1984

Adoptive transfer of acquired resistance to Mycobacterium kansasii by T cells harvested from chronically-infected mice.

Growth of Mycobacterium kansasii in intravenously infected mice ceases when the spleen cells express an enhanced non-specific resistance to a secondary challenge. Mice inoculated with 10(6) CFU M. kanasii 1203 develop a population of splenic T cells which are able to transfer protection passively to sublethally-irradiated syngeneic recipients when challenged with M. kansasii. Although the T-cell activated macrophages were unable to eliminate the mycobacteria from the spleen, they were able to prevent further growth of the organism in vivo. When mice which lack T cells (congenitally athymic, or 'nude' mice) were infected with M. kansasii, the cellular defences were unable to halt the progressive growth of the challenge organisms within the tissues. When normal mice were inoculated with large numbers of viable M. kansasii 1203 (up to 5 X 10(7) CFU), the activated macrophages within the spleen were capable of limiting the further growth of the bacterial population in vivo, but with no T-cell response capable of adoptively immunizing naive recipients against a secondary M. kansasii challenge. Thus, it seems likely that M. kansasii can induce the formation of activated macrophages by two separate mechanisms: one is a T-cell dependent process which occurs in mice inoculated with moderate doses (10(6) CFU) of M. kansasii, while the other is T-cell independent and occurs when a large infectious inoculum is employed.

Animals↗
PubMedDate not supplied

Modulation of experimental autoimmune uveoretinitis by adoptive transfer of cells from rats immunized with anti-S-antigen monoclonal antibody.

Preimmunization of rnu/+ rats with the mouse monoclonal antibody S2D2 against retinal S-antigen (S-Ag) leads to an anti-idiotypic (anti-Id) response and to protection against experimental autoimmune uveoretinitis (EAU) provoked by a subsequent challenge with S-Ag in complete Freund's adjuvant (CFA). Suppression of EAU can be passively transferred using lymph node and/or spleen cells from donors with active anti-Id immunity to naive rnu/+ recipients, prior to immunization with bovine S-Ag in CFA. In contrast, passive administration of IgG from S2D2-immunized rats did not produce suppression. High levels of anti-Id S2D2 antibodies were found: (1) in rats presenting an inhibited EAU after sensitization with S2D2 or after passive transfer of anti-S2D2 cells prior to the S-Ag immunization; and (2) in rats with a severe EAU after transfer of anti-S2D2 IgG associated with anti-S2D2 cells prior to the S-Ag challenge. No effect on the anti-S-Ag antibody level could be detected. These experiments suggest that EAU, a mostly T cell-dependent disease, can be down regulated by anti-Id lymphoid cells.

Animals↗
PubMed1996

Elimination of established liver metastases by human interleukin 2-activated natural killer cells after locoregional or systemic adoptive transfer.

An in vivo model of liver metastasis induced by human gastric carcinoma was established in nude mice and used for locoregional or systemic immunotherapy with a subset of human A-natural killer (NK) cells defined previously. A single intrasplenic (i.s.) delivery of A-NK cells (1 x 10(7)) and interleukin 2 (IL-2; 60,000 international units, twice a day for 5 days, i.p.) to animals with 3-day established liver metastases, but not IL-2 alone, resulted in rapid (within 24 h) elimination of the majority of metastases and significantly improved survival. A single i.s. or i.v. transfer of these effector cells and IL-2 significantly prolonged survival of the mice with 3-day established metastases (P < 0.03 and P < 0.02, respectively) compared with untreated mice. Using 51Cr-labeled A-NK cells, it was determined that, at best, 75% of 1 x 10(7) cells delivered i.s., and up to 50% of those delivered i.v. were found in the liver 30 min-4 h later. Using image analysis with Di-O dye-labeled A-NK cells, 60-100% of A-NK cells delivered i.s. or i.v. were detected in the liver 24 h later. By light microscopy, 3-day liver metastases were mostly intravascular, but some had already begun to spread into liver tissue. When rhodamine- or Di-O dye-labeled A-NK cells were injected i.s. or i.v. to study their distribution in the liver, they were detectable by confocal fluorescence microscopy in tumor-free tissue and in association with tumor cells 12-24 h after transfer. No evidence for selective localization of A-NK cells to liver metastases was obtained; many A-NK cells were randomly distributed in tissue and not associated with visible metastases. However, confocal fluorescence and electron microscopy showed some A-NK cells to be in cell-to-cell contact with tumor cells, both in the blood vessel and liver tissue. These results indicate that a majority of human A-NK cells transferred i.s. or i.v. to mice with liver metastases have the capacity to migrate to the liver and to enter liver tissue and tumor metastases in vivo. The presence of these effector cells even in a modest number in the liver leads to elimination of most, but not all, metastases and to significantly prolonged survival of animals treated with A-NK cells and IL-2.

Animals↗
PubMed2002

Resolution of chronic hepatitis B and anti-HBs seroconversion in humans by adoptive transfer of immunity to hepatitis B core antigen.

BACKGROUND & AIMS: Impaired T-cell reactivity is believed to be the dominant cause of chronic hepatitis B virus (HBV) infection. We characterized HBV-specific T-cell responses in chronic hepatitis B surface antigen carriers who received bone marrow from HLA-identical donors with natural immunity to HBV and seroconverted to antibody to hepatitis B surface antigen. METHODS: T-cell reactivity to HBV antigens and peptides was assessed in a proliferation assay, the frequency of HBV core- and surface-specific T cells was quantified directly by ELISPOT assays, and T-cell subsets were analyzed by flow cytometry. RESULTS: CD4+ T-cell reactivity to HBV core was common in bone marrow donors and the corresponding recipients after hepatitis B surface antigen clearance, whereas none reacted to surface, pre-S1, or pre-S2 antigens. Furthermore, CD4+ T cells from donor/recipient pairs recognized similar epitopes on hepatitis B core antigen; using polymerase chain reaction for the Y chromosome, the recipients' CD4+ T lymphocytes were confirmed to be of donor origin. The frequency of core-specific CD4+ and CD8+ T cells was several-fold higher than those specific for surface antigen. CONCLUSIONS: This study provides the first evidence in humans that transfer of hepatitis B core antigen-reactive T cells is associated with resolution of chronic HBV infection. Therapeutic immunization with HBV core gene or protein deserves further investigation in patients with chronic hepatitis B.

Adolescent↗
PubMed1996

Lymphocyte function associated antigen-1, integrin alpha 4, and L-selectin mediate T-cell homing to the pancreas in the model of adoptive transfer of diabetes in NOD mice.

The involvement of adhesion molecule in the process of T-cell homing to the pancreas was investigated in the model of the T-cell transfer of type I diabetes in NOD mice. Treatment of mice using monoclonal anti-lymphocyte function associated antigen (LFA)-1, anti-integrin alpha 4, anti-intercellular adhesion molecule (ICAM)-1, and anti-L-selectin antibodies (monoclonal antibodies [mAbs]) gave rise to a partial or complete prevention of diabetes via different mechanisms of protection. On day 20 posttransfer, diabetes was only observed in control mice (26 of 32) and in few mice treated with the anti-L-selectin mAbs (3 of 24). On day 60, the best protection was observed using the anti-LFA-1 or the anti-integrin alpha 4 mAbs with 3 of 11 and 2 of 5 diabetic mice, respectively. On day 20, no insulitis was observed in the pancreases of mice treated with these mAbs compared with the pancreases of controls, suggesting that such treatment blocked the penetration of T-cells into the islets. In vitro adhesion assays confirmed that adhesion of T-cells to the pancreatic endothelium was blocked, except when using the anti-L-selectin mAb, which induced a modification of the traffic of the transferred T-cells; the ability of T-cells to migrate into the pancreatic lymph nodes was significantly reduced (10.4 vs. 22%). Anti-LFA-1 mAbs did not modify such T-cell trafficking. The present study, therefore, elucidates the role of LFA-1, integrin alpha 4, and L-selectin in T-cell homing to the pancreas, first step of the cascade of events leading to type I diabetes.

Animals↗
PubMed1991

Adoptive transfer of neonatal T lymphocytes rescues immunoglobulin production in mice with severe combined immune deficiency.

Mice with the autosomal recessive severe combined immune deficiency (scid) mutation lack mature lymphocytes because of defective joining of T cell receptor and immunoglobulin (Ig) gene segments. Penetrance of this mutation is incomplete since 10-25% of SCID mice produce some T or B lymphocytes. This "leaky" phenotype could be due to a reversion of the mutation in some mice or to a constant, low frequency of functional lymphocytes generated in all SCID mice with variable survival of such cells. We report here that all SCID mice can be stimulated to produce functional B cells by the transfer of normal neonatal, but not adult, T cells. T cell-induced rescue of C.B-17scid B cells results in high levels of Ig expressing the Ighb allotype of the SCID recipient. These results show that all SCID mice generate some functional B cells, the majority of which do not survive in the absence of a subset of T cells present in high frequency in the neonate.

Aging↗
PubMed1991

Strong priming of T cells adoptively transferred into scid mice.

We have examined the requirements for activating unprimed T cells in vivo by transferring T cells into scid mice, which lack mature B and T cells. Purified adult thymocytes and a protein antigen, keyhole limpet hemocyanin (KLH), were injected into scid mice. scid mice injected with T cells and KLH developed cellular lymph nodes containing CD4+ and CD8+ T cells. Cells recovered from the lymph nodes of injected scid mice proliferated and secreted interleukin 2 in response to KLH in vitro. The results indicate that T cells can be primed to KLH in the scid mouse in the absence of B cells.

Animals↗
PubMed2003

Adoptive transfer of an anti-MART-1(27-35)-specific CD8+ T cell clone leads to immunoselection of human melanoma antigen-loss variants in SCID mice.

The identification of appropriate mouse models could be useful in carefully evaluating the actual role of the in vivo development of antigen-loss variants during antigen-specific vaccine therapy of human tumors. In this study we investigated the level of efficacy of a MART-1/Melan-A-specific CD8+ T cell clone against its autologous melanoma in a severe combined immunodeficiency (SCID) mouse model, in which the tumor cells expressed in vivo heterogeneous and suboptimal levels of MART-1. The subcutaneous co-injection of the MART-1/Melan-A-reactive T cell clone A42 with MART-1/Melan-A+ autologous human melanoma cells into SCID mice caused a total inhibition of tumor growth. However, the systemic treatment with A42 clone lymphocytes resulted in only 50-60% inhibition of tumor growth, although the T cell clone targeted the tumors and the MART-1+ cells virtually disappeared from the tumors. This study suggests that an immunotherapy based on the expansion of an antigen-specific T cell clone generated in vitro is highly efficient in abolishing tumor growth when the target antigen is fully expressed, but leads to in vivo immunoselection of antigen-loss variants in the presence of suboptimal levels of antigen expression. Furthermore, this work shows that human tumors/SCID mouse models may be useful in evaluating the in vivo efficacy of adoptive immunotherapies.

Animals↗
PubMed2002

Do not underestimate the power of antibodies--lessons from adoptive transfer of antibodies against HIV.

Successes for neutralizing antibodies (nAbs) against the human immunodeficiency virus (HIV) include potent cross-clade neutralization of primary virus isolates by human neutralizing monoclonal antibodies (nmAbs) targeting conserved envelope epitopes. Furthermore, passively administered combinations of human nmAbs prevented infection in primates, indicating that epitopes recognized by such nmAbs are key determinants for protection. Lastly, in the absence of CD8+ T cells, nAbs may act as a second line of defense during chronic infection. Taken together, these results argue for generating nAb response-based prophylactic and/or therapeutic AIDS vaccines. We suggest that the epitopes identified by passive immunization represent excellent targets for the rational design of nAb response-based AIDS vaccines.

Acute Disease↗
PubMed1992

Adoptive transfer of skin-selective autoimmunity induced by Skn alloantigenic disparities.

Two unlinked genes of the mouse, Skn-1 and Skn-2, each with alterative alleles, specify alternative cell-surface Skn alloantigens expressed only by epidermal and neural cells. C57BL/6 (B6) and A/J (A) strain mice differ at both Skn loci. Thus lethally irradiated B6 mice restored with (B6 x A)F1 hybrid hematopoietic cells [(B6 x A)/B6 chimeras] reject A strain (Skn-incompatible) skin grafts. Our studies were designed primarily to test the inference that (B6 x A)F1 lymphoid cells, after differentiating in B6 recipients, which lack the Skn alloantigens of A strain mice, may make an Skn-related, skin-selective autoimmune response when returned to their native (B6 x A)F1 habitat. Severe cutaneous lesions did, indeed, ensue after spleen cells of (B6 x A)/B6 chimeras were transferred to (B6 x A)F1 recipients, provided that three conditions were met--namely, (i) priming of the (B6 x A)/B6 chimeric donor by grafting and rejection of Skn-incompatible A strain skin grafts, (ii) stimulation of the recipient's skin as from shaving, at which sites the lesions were mainly located, and (iii) pretreatment of the (B6 x A)F1 recipients with cyclophosphamide or sublethal irradiation. Spleen cells of control female chimeras primed by grafting and rejection of H-Y (Skn-compatible) B6 male skin failed to incite the Skn-typical cutaneous lesions in (B6 x A)F1 recipients, indicating that these lesions were Skn-specific and not a nonspecific consequence of incompatible skin grafting per se. Normally compatible A strain skin grafts, but not Skn-compatible B6 skin grafts, were rejected by cyclophosphamide-treated (B6 x A)F1 recipients of (B6 x A)/B6 spleen cells from Skn-primed chimera donors. Treatment of primed chimeras' spleen cells with antiserum to H-2a (A strain) specifically abolished their capacity to adoptively incite the Skn-related autoimmune syndrome, confirming that the immune cells responsible are of (B6 x A)F1 origin and are not residual B6 derivatives. These findings add weight to the status of Skn systems as agents of tissue-selective histoincompatibility and, perhaps, of clinical disorders with a known or suspected autoimmune basis affecting the skin.

Alleles↗
PubMed1994

Analysis of the adoptive transfer of delayed hypersensitivity and T cell repertoire in severe combined immunodeficiency mice reconstituted with human lymphocytes.

The functional capacity of human T cells to passively transfer delayed hypersensitivity (DH) was analysed in severe combined immunodeficiency (SCID) mice. The tissue distribution of human peripheral blood lymphocytes (PBL) was analysed by 51chromium labelling 1 and 24 h after intravenous cell injection. Labelled PBL from purified protein derivative (PPD)-positive healthy individuals mainly localize in the spleen, liver and lungs, with no arrival in the peripheral lymphoid organs and at the site of antigen challenge (footpad). According to such defective distribution, human PPD-immune cells failed to passively transfer PPD-specific DH to SCID recipients when cells were injected either intravenously or intraperitoneally (systemic transfer). On the contrary, PPD-immune cells were able to transfer DH to PPD when injected directly into the footpad (local transfer). Both memory (CD45RA-) and naive (CD45RA+) enriched subsets were equally able to transfer local DH. The long-term reconstitution of the human immune system in SCID mice was analysed after intraperitoneal PBL transfer (hu-PBL-Scid) by phenotypic analysis, immunoglobulin level, and human DNA detection. Moreover, the reconstitution of the V beta T cell receptor (TCR) repertoire in SCID mice was analysed by anchored polymerase chain reaction (PCR) showing that all the 22 V beta families were expressed in the spleen of hu-PBL-SCID mice. Moreover, scanner analysis of Southern blotting revealed the selective expansion of distinct V beta families (V beta 3, V beta 6, V beta 8, V beta 13.1, V beta 14, V beta 17), suggesting that human lymphocytes could recognize specific antigens or superantigens in the SCID environment.

Animals↗
PubMedDate not supplied

Adoptive transfer of activated human autologous macrophages results in regression of transplanted human melanoma cells in SCID mice.

The potential anti-tumor activity of human macrophages, grown in macrophage colony stimulating factor (M-CSF), was examined in mice homozygous for the mutation severe combined immune deficiency (scid) bearing xenografts of autologous human melanoma. Injection of scid mice, bearing subcutaneous melanoma xenografts, with the cultured macrophages or with the macrophage culture supernatant, once or repeatedly, resulted in partial to complete regression of tumors. Since a large number of such macrophages (greater than 1 x 10(9)) could be grown in vitro for repeated injection, the scid-human chimera can serve as an in vivo model to examine the role of human macrophages in tumor immunity and to explore the potential of the in vitro cultured macrophages in the therapy of cancer.

Animals↗
PubMed1995

Production of genetically modified Epstein-Barr virus-specific cytotoxic T cells for adoptive transfer to patients at high risk of EBV-associated lymphoproliferative disease.

EBV-induced lymphoproliferative disease (EBV-LPD) is a disorder most commonly associated with the immunocompromise that follows allogeneic organ transplantation. In patients receiving T cell-depleted bone marrow from HLA-mismatched or HLA-matched unrelated donors, the incidence of EBV-LPD is particularly high, ranging from 5 to 30%. Administration of EBV-specific cytotoxic T lymphocytes may be one means of preventing and treating this disease. We now describe a method that allows the routine and timely preparation of large numbers of such cells to allow their safe administration to bone marrow transplant recipients. We also describe how these cells may be genetically marked before infusion, to determine their fate and disposition in vivo.

Adolescent↗
PubMed2003

[Analysis of 5-year survival among breast cancer patients with malignant pleural effusion receiving intrapleural OK-432 followed by adoptive transfer with cultured effusion lymphocytes].

Since 1984, we have had 151 breast cancer patients with cytologically-confirmed malignant pleural effusions by local transfer of autologous effusion lymphocytes cultured with a conditioned medium containing T-cell growth factor after intrapleural preadministration of a streptococcal preparation, OK-432. Among the 81 patients given this therapy more than 5 years ago, 12 patients have survived 5 or more years, and 4 of these 12 have survived 10 (<) years. Patients surviving 5 (<) years had longer (32-204 months) disease-free periods, except for one patient with stage IV disease. Estrogen receptor was positive in 5 patients, negative in 1 patient, and unknown in 6 patients. Moreover, preceding or concomitant metastases in these patients were not life-threatening (6 chest-wall, 2 lymph-node, 4 lung, 3 bone metastases). In conclusion, effective therapy (effusion disappeared in all patients) and good control of concomitant metastases resulted in long-term survival of patients who had intrinsically better prognostic factors.

Adult↗
PubMed1991

[The therapeutic use of diucifon-activated immunocytes in adoptive transfer in mice with burn trauma complicated by Pseudomonas aeruginosa infection].

The effectiveness of the therapeutic use of diucyphone-stimulated syngeneic spleen cells was studied in mice with a burn trauma complicated by P. aeruginosa infection. For this purpose CBA mice were subjected to a burn of degree IIIa, covering 30% of their body surface, the wound was infected with P. aeruginosa strain, and 24 hours later spleen cells were taken from some of these animals. The spleen cells, incubated for 3 hours with or without diucyphone at a concentration of 10-100 micrograms/ml, were washed and reinfused intravenously to the remaining animals. The injection of diucyphone-treated spleen cells was shown to greatly increase the survival rate of the animals, to accelerate healing processes and to enhance the proliferative response of spleen cells to mitogens (phytohemagglutinin, concanavalin A) and interleukin-2. A conclusion was made on the efficacy of the therapeutic use of diucyphone-activated immunocompetent cells in cases of immunodeficiency induced by burn infection.

Adjuvants, Immunologic↗
PubMed1992

Adoptive transfer of the gld syndrome in double congenic nude lpr mice.

Homozygosity for either the lymphoproliferation (lpr) or the generalized lymphoproliferative disease (gld) mutation of mice causes the development of strikingly similar autoimmune and lymphoproliferative syndromes. The relationship between the lpr and gld mutations was studied by grafting B6 gld spleen cells (SC) to athymic B6 nude lpr mice (B6 nulpr) or to B6 nude (B6 nu) mice as controls. The injection of B6 gld SC, but not of B6 wild SC, to B6 nulpr mice caused a prolongation of survival of the short living B6 nulpr recipients. This was associated with elevated anti-single stranded DNA antibody titers and a serum hyperglobulinemia, as well as by a splenomegaly which was nearly as high as in genetically B6 gld mice, and by a marked lymphadenopathy (though milder than that of B6 gld mice). In contrast the [gld----nu] chimaeras showed a more attenuated form of gld-induced syndrome. These results suggest that the lpr environment supplied in athymic lpr recipients is compatible with--and may even favour--the development of the gld-induced syndrome.

Animals↗