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PubMed1998

Adoptive transfer: the role of perforin in mouse cytotoxic T lymphocyte rejection of human tumor xenografts in vivo.

The popliteal lymph node cells of immunocompetent mice generated a strong in vitro cytotoxic response to footpad injection of several human tumor cell lines and the resulting mouse effector cells predominantly used a perforin-mediated cytotoxic mechanism. A relatively minor FasL-dependent cytotoxic response to CEM-CCRF and Jurkat leukemias, but not colon carcinoma COLO 205 cells, was also detected in immunized perforin-deficient mice. In vitro depletion of CD3+ CD8+ T cells, but not CD4+ T or NK1.1+ cells, completely inhibited lysis of human tumor cells, suggesting that CD3+ CD8+ T cells were effectors of perforin-mediated xenospecific cytotoxicity. Xenospecific cytotoxic T cells from wild-type mice were extremely efficient at rejecting tumor when adoptively transferred into scid mice bearing established COLO 205, CEM-CCRF, or Jurkat tumor xenografts. By contrast, cytotoxic T lymphocytes of perforin-deficient mice had no effect on the growth of established tumor xenografts. These data indicate that perforin, and hence direct cytotoxicity, plays a key role in the ability of adoptively transferred CD8+ cytotoxic T lymphocytes to eradicate established xenografts.

Adoptive Transfer↗
PubMed1982

Immunologic requirements for the adoptive transfer of ectromelia virus meningitis.

Intracerebral infection with the Hampstead egg strain of ectromelia virus in mice produced a meningitis with clinical signs and death. A single injection of cyclophosphamide three days after infection delayed the onset of pathology and clinical signs. Adoptive transfer of immune spleen cells into preinfected recipients could induce the meningitis earlier. These donor-immune cells were virus-specific in their action. The Ig- population, deficient in B lymphocytes, could transfer meningitis; but donor-immune cells depleted of T lymphocytes by anti-theta treatment or the Ig+ population, deficient in T-cells, were unsuccessful. Studies with labeled cells showed a preferential accumulation of labeled donor cells in cerebrospinal fluid in the first 24 hours post-transfer, whereas labeled recipient cells accumulated between 24 and 48 hours. The results demonstrated that the adoptive transfer of ectromelia virus meningitis was a cell-mediated inflammatory process.

Animals↗
PubMed1981

Adoptive transfer of total and parasite-specific IgE responses in rats infected with Nippostrongylus brasiliensis.

Infection of rats with Nippostrongylus brasiliensis has both a parasite-specific and non-specific IgE stimulating effect. Both these responses can be adoptively transferred with thoracic duct lymphocytes (TDL) from infected rats. The character of the IgE response in the recipient rats was related to the stage after infection of the cell donors. TDL from hyperimmune rats adoptively transferred high serum titres of parasite-specific IgE to infected recipient rats and substantially increased the levels of total IgE. However, adoptive immunization with TDL from donors infected 10 days previously did not stimulate parasite-specific IgE and only slightly increased total IgE levels. After cell fractionation the sIg- cells from day 10 TDL increased the level of total IgE but not parasite-specific IgE whereas sIg- cells from hyperimmune TDL did not induce any IgE response unless given with sIg+ cells. The possible reasons for this are discussed.

Animals↗
PubMed1997

Induction of degenerative brain lesions after adoptive transfer of brain lymphocytes from Borna disease virus-infected rats: presence of CD8+ T cells and perforin mRNA.

Lymphocytes were isolated from the brains of Borna disease virus-infected donor Lewis rats at various time points after infection. Cell populations were characterized by cytofluorometry, with special emphasis on CD4+ and CD8+ cells. Testing of isolated lymphocytes revealed major histocompatibility complex class I-restricted cytotoxic activity. Reverse transcription-PCR analyses of brain homogenates of infected donors revealed the presence of CD8 mRNA after day 11 of infection and of perforin mRNA between days 13 and 25 after infection. Adoptive transfers of lymphocytes isolated from the brain at days 13 and 21 resulted in severe neurological symptoms, resembling experimental Borna disease. The onset of disease was dependent on the cell numbers transferred and was clearly related to the appearance of T cells in the brain. CD8+ T cells were found in the parenchyma, whereas CD4+ T cells were found predominantly in perivascular locations. A disseminated lymphocytic infiltration in the parenchyma was accompanied by severe morphological alterations, including significant necrosis of neurons. Furthermore, a prominent spongiform-like degeneration was observed; this increased over time and finally resulted in severe cortical brain atrophy. Lymphocytes obtained during the beginning chronic phase of experimental Borna disease in rats had no significant cytolytic capacity in vitro and were also not able to induce neurological symptoms typical of Borna disease after adoptive transfer. The data presented here show for the first time that lymphocytes isolated from the site of the inflammatory lesions, namely, the brains of diseased rats, induce the immunopathological reaction and cause Borna disease. After transfer, the pathological alterations induced in the recipients exactly reflect those observed during experimentally induced Borna disease in rats, including necrosis of neurons and glial cells and gross degeneration resulting in cortical brain atrophy. Evidence that the immunopathology of Borna disease is closely related to the presence of CD8+ T cells in the brain parenchyma is provided.

Adoptive Transfer↗
PubMed2003

Development of autoimmune exocrinopathy resembling Sjögren's syndrome in adoptively transferred mice with autoreactive CD4+ T cells.

OBJECTIVE: The pathologic mechanisms responsible for organ-specific tissue damage in primary Sjögren's syndrome (SS) remain unclear, but it has been suggested that the pathology is mediated by autoreactive CD4+ T cells infiltrating the salivary and lacrimal glands. This study was undertaken to investigate whether alpha-fodrin autoantigen-specific autoreactive CD4+ T cells are capable of inducing autoimmune lesions. METHODS: A total of 45 synthetic alpha-fodrin peptides designed to be 20 amino acid residues in length were generated. To establish an autoreactive T cell line, limiting dilution analysis (LDA) was performed on lymph node cells (LNCs) in the presence of alpha-fodrin peptides. The effects of adoptive transfer of autoreactive CD4+ T cells into normal syngeneic recipients were investigated. RESULTS: Autoreactive CD4+ T cell lines that recognize synthetic alpha-fodrin peptide, which produced Th1 cytokines and showed cytotoxic activities, were established in a murine model for SS. T cell receptor V(beta) usage and third complementarity-determining region (CDR3) sequences indicated that in some cases V(beta)6-CDR3 genes matched between the tissue-infiltrating T cells and the autoreactive T cell lines. Adoptive transfer of the autoreactive CD4+ T cells into normal syngeneic recipients induced autoimmune lesions quite similar to those of SS. CONCLUSION: Our data help to elucidate the pathogenic mechanisms responsible for tissue destruction in autoimmune exocrinopathy and indicate that autoreactive CD4+ T cells play a pivotal role in the development of murine SS.

Adoptive Transfer↗
PubMed2003

Adoptive transfer of mast cells abolishes the inflammatory refractoriness to allergen in diabetic rats.

Mast cells are pivotal secretory cells primarily implicated in allergen-evoked inflammatory responses and are downregulated following experimental chemical diabetes. Here we tested the hypothesis that a decrease in the number and reactivity of mast cells would account for the hyporesponsiveness of diabetic rats to allergen-induced inflammation. We found that the anaphylactic release of histamine from sensitized ileum, trachea and skin tissues was clearly reduced in rats turned diabetic via intravenous administration of alloxan. Likewise, actively and passively sensitized diabetic rats mounted a weaker allergen-evoked pleural mast cell degranulation and protein extravasation, as compared to sensitized nondiabetic animals, which paralleled a marked reduction in the mast cell population in the pleural cavity. The number of mast cells enumerated in the mesentery from diabetic rats was also clearly reduced. The allergen-evoked plasma leakage in diabetic rats was restored by the transfer of mast cells from sensitized nondiabetic rats. Moreover, the adoptive transfer of sensitized mast cells from diabetics to naive animals led to a lower allergen-induced exudation as compared to the response noted after the transfer of sensitized naive mast cells. Purified mast cells from diabetic rats were hyporesponsive to antigen and compound 48/80 stimulation in vitro as attested by histamine release. Thus, our results show that the phenomenon of refractoriness of diabetic animals to allergen challenge appears to be accounted for by a reduction in the number and reactivity of mast cells.

Adoptive Transfer↗
PubMed1998

Experimental autoimmune myocarditis produced by adoptive transfer of splenocytes after myocardial infarction.

One possible mechanism for neurohumoral activation after myocardial infarction may be the generation of an immune response against cardiac self-antigens. We hypothesize that if there is a T cell-mediated reaction to self-antigens, the transfer of splenic lymphocytes from postinfarct rats into syngeneic rats with normal hearts should result in a T cell-mediated autoimmune myocarditis in the healthy syngeneic rats. Rats were killed 6 weeks after coronary ligation. Splenocytes from animals with large and small infarcts were purified from spleens, activated with concanavalin A, and injected in varying doses into normal syngeneic rats. These recipient rats were killed 6 weeks later, and histopathological studies were performed. Our results demonstrate in vivo evidence of lymphocyte-mediated myocardial injury by adoptive transfer of sensitized lymphocytes from rats who developed congestive heart failure after acute myocardial infarction. The amount of infiltrate and necrosis in the recipient rats appeared directly related to the size of the infarct from the donor rats. This suggests that larger infarcts lead to a greater inflammatory response as well as a greater propensity for alteration of cardiac surface antigens or the emergence of previously sequestered antigens. None of the other organs (kidney, liver, lung, or brain) had evidence of infiltrates. Two-dimensional echocardiography did not reveal systolic dysfunction. This study provides direct evidence of autoimmune myocardial injury produced by adoptive transfer of concanavalin A-activated splenocytes after myocardial infarction. We propose that neurohumoral activation early in the postinfarction period triggers a series of specific inflammatory and immunological events that lead to formation of specific clones of T cells. When these are activated and transferred into normal rats, cardiac-specific cellular infiltration occurs, occasionally accompanied by myocardial necrosis. This model should help to further explore the link between neurohumoral activation after myocardial infarction and the subsequent immune alterations that might be associated with the development and/or progression of congestive heart failure. Additionally, this might be a useful model in which to study other immune-mediated cardiomyopathies.

Adoptive Transfer↗
PubMed1987

The immunopathology of adoptively transferred experimental allergic encephalomyelitis (EAE) in Lewis rats. Part 1. Immunohistochemical examination of developing lesions of EAE.

In order to examine developing lesions of experimental allergic encephalomyelitis (EAE) at the preclinical stage, adoptive transfer of EAE was achieved in Lewis rats using spleen cells obtained from rats previously immunized with 50 micrograms of guinea pig myelin basic protein (MBP) in complete Freund's adjuvant. After cell transfer, all the recipient rats developed severe paraparesis with minimal variation in the onset of clinical signs, which facilitated immunohistochemical examination of developing lesions of EAE in asymptomatic animals. The initial pathological finding detected in this system was an increased number of inflammatory cells (both OX19+ and OX8+ T cells and macrophages) in the subarachnoid space (SAS) which was observed on day 3 post-transfer (PT) when the recipient animals showed no neurological abnormalities. By day 4 PT, inflammatory cells were detected in the Virchow-Robin space of vessels which were continuous to the SAS. Perivascular lymphocytic infiltration was scarcely detected in the gray matter. On day 5 PT, the rats showed severe paraparesis. Inflammatory foci increased in number and were detected in both the white and gray matter. Diffuse parenchymal T-lymphocyte infiltration was also recognized at this stage. From day 6 PT onwards, inflammatory cells decreased gradually. On day 8 PT, all the rats recovered from EAE and few inflammatory cells were detected in the parenchyma and SAS. Immunohistochemical examination of T-cell subsets and Ia antigens revealed that the number of OX19+ cells was greater than that of OX8+ cells in the parenchyma and SAS at all stages examined, the distribution of OX19+ cells was almost the same as that of OX8+ cells, OX8+ cells decreased in number before clinical signs subsided, and that after the infiltration of T cells into the parenchyma, cells with dendritic morphology (microglia) expressed Ia antigens in close association with the infiltrating T cells. Adoptive transfer of MBP-sensitized spleen cells provides constant induction of EAE with minimal variation in clinical onset and severity, thus being a useful model for the examination of early events of EAE.

Albumins↗
PubMed1985

Comparative immunohistologic studies in an adoptive transfer model of acute rat cardiac allograft rejection.

It has been shown that fulminant acute rejection of rat cardiac allografts across a full haplotype disparity may occur as a direct result of adoptive transfer of sensitized W3/25+ MRC OX8- SIg- T helper/DTH syngeneic spleen cells to sublethally irradiated recipients. In order to establish the immunohistologic parameters of this form of rejection, allografts and recipient lymphoid tissue were analyzed using a panel of monoclonal antibodies of known cellular distribution. These data were compared with those obtained following reconstitution of irradiated allograft recipients with unseparated sensitized spleen cells, with unreconstituted irradiated donor recipient pairs, with unmodified first-set rejection, and with induced myocardial infarction of syngeneic heart grafts transplanted to normal and to sublethally irradiated recipients. Rejecting cardiac allografts transplanted to all reconstituted irradiated recipients were characterized by extensive infiltration with MRC OX8+ (T cytotoxic-suppressor, natural killer) cells even when this subset was virtually excluded from the reconstituting inocula. A similar proportional accumulation of MRC OX8+ cells observed at the infarct margins of syngeneic heart grafts transplanted to irradiated unreconstituted recipients greatly exceeded that present in normal nonirradiated controls. These data provide evidence that under conditions of heavy recipient irradiation, MRC OX8+ cells may be sequestered within heart grafts in response to nonspecific injury unrelated to the rejection process. Although there was no significant degree of MRC OX8+ cellular repopulation within organized secondary lymphoid tissues of irradiated animals over the study period, the density of ileal mucosal MRC OX8+ lymphocytes approximated normal at 7 days post-irradiation, raising the possibility that these cells could share a common origin with those sequestered within the heart grafts. Carbon+ MRC OX6+ macrophages were a significant component of the infiltrate in all rejecting cardiac allografts, as well as in all infarcted syngeneic heart grafts--providing further evidence that macrophage "activation" with expression of class II determinants may occur in response to nonspecific injury. In unmodified first-set rejection there was an intense B cell reaction in recipient spleens and lymph nodes. In the adoptive transfer model, marked B cell expansion was exclusively confined to the parathymic lymph nodes of irradiated allograft recipients reconstituted with the sensitized W3/25+, MRC OX8-, SIg- T helper/DTH donor cell inocula.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Immune response of mice to sarcoma I allograft studied by adoptive transfers of spleen, thymus, and lymph node cells to secondary recipients.

Thymus, spleen, and lymph node cells from different periods of Sarcoma I allograft development in untreated (Sa I) or xenogeneic antithymocyte serum-treated (ATS-Sa I) B10 mice were adoptively transferred to secondary B10 recipients. While in sublethally (4.3 Gy) irradiated recipient mice the tumor destructing activity was predominantly expressed, in untreated recipients of transferred cells it was mostly the tumor enhancing activity. Therefore, in further studies directed at the detection of tumor enhancing activity, the adoptive transfers were only performed in untreated recipients. Thymus cells both of Sa I and ATS-Sa I mice showed a tumor enhancing activity all through the followed period, with a peak between days 7 and 21, then it decreased. Also the spleen cells of both groups had a tumor enhancing effect all the time, with a peak of activity on day 7. Spleen and thymus cells of progressors enhanced the tumor growth slightly more strongly than did those of the regressors. The tumor enhancing activity of spleen cells was in the beginning period confined mainly to the polystyrene nonadherent fraction of cells, at later times, in the progressors it was manifested in the adherent as well as in the nonadherent fractions. In the population of lymph node cells, at the start of tumor regression (in Sa I mice on day 7, in ATS-Sa I mice on day 14), a tumor destructing activity was observed. In both groups this activity was at later times followed by a tumor enhancing activity. The interpretation of the tumor enhancing activity of thymus and spleen cells of Sa I and ATS-Sa I mice is complicated by the tumor enhancing activity of cells of normal mice without tumor (N).

Animals↗
PubMed2001

Indirect allorecognition in acquired thymic tolerance: induction of donor-specific permanent acceptance of rat islets by adoptive transfer of allopeptide-pulsed host myeloid and thymic dendritic cells.

Pancreatic islet transplantation remains a promising approach to the treatment of type 1 diabetes. Unfortunately, graft failure continues to occur because of immunologic rejection, despite the use of potent immunosuppressive agents. It is therefore reasoned that induction of peripheral tolerance by the use of self-dendritic cells (DCs) as a vehicle to deliver specific target antigens to self-T-cells without ex vivo manipulation of the recipient is an attractive strategy in the treatment of type 1 diabetes. The finding that intrathymic inoculation of an immunodominant WF major histocompatibility complex (MHC) Class I (RT1.A(u)) peptide five (P5) or P5-pulsed host myeloid DCs induces acquired thymic tolerance raises the possibility that adoptive transfer of allopeptide-primed host myeloid or lymphoid DCs might induce transplant tolerance. To address this hypothesis, we studied the effects of intravenous transfer of in vitro P5-pulsed syngeneic myeloid DCs or in vivo P5-primed syngeneic lymphoid (thymic) DCs on islet survival in the WF-to-ACI rat combination. In vivo primed thymic DCs isolated from ACI rats given intrathymic inoculation of P5 for 2 days were capable of in vitro restimulation of in vivo P5-primed T-cells (memory cells). In the first series of studies, we showed that intravenous-like intrathymic-inoculation of in vitro P5-pulsed host myeloid DCs induced donor-specific permanent acceptance of islets in recipients transiently immunosuppressed with antilymphocyte serum (ALS). We next examined whether thymic DCs isolated from animals that had been previously intrathymically inoculated with P5 could induce T-cell tolerance. The results showed that intravenous adoptive transfer of in vivo P5-primed thymic DCs led to donor-specific permanent acceptance of islets in recipients transiently immunosuppressed with ALS. This finding suggested that the thymic DCs take up and present P5 to developing T-cells to induce T-cell tolerance, thus providing evidence of a direct link between indirect allorecognition and acquired thymic tolerance. The second series of studies examined the mechanisms involved in this model by exploring whether in vivo generation of peptide-specific alloreactive peripheral T-cells by intravenous inoculation of P5-pulsed self-DCs was responsible for the induction of T-cell tolerance. Intrathymic inoculation of splenic T-cells obtained from syngeneic ACI rats primed with intravenous injection of P5-pulsed DCs with a high in vitro proliferative response to P5 in the context of self-MHC induced donor-specific permanent acceptance of islets from WF donors. In addition, the clinically relevant model of intravenous injection of P5-activated T-cells combined with transient ALS immunosuppression similarly induced transplant tolerance, which was then abrogated by thymectomy of the recipient before intravenous injection of the activated T-cells. These data raise the possibility that circulation of peptide-activated T-cells to the host thymus plays a role in the induction and possibly the maintenance of T-cell tolerance in this model. Our findings suggest that intravenous administration of genetically engineered host DCs expressing alloMHC peptides might have therapeutic potential in clinical islet transplantation for the treatment of autoimmune diabetes.

Adoptive Transfer↗
PubMed1986

Irradiated lymphocytes do not adoptively transfer diabetes or prevent spontaneous disease in the BB/W rat.

Diabetes in the BB/W rat is autoimmune in origin, and lymphocytes from acutely diabetic animals activated by concanavalin A (con A) induce the disease in adoptive recipients. We report that irradiation of these cells prevents adoptive transfer of diabetes. Through 60 days of age, diabetes occurred in none of 47 BB/W rats given irradiated con A cells, but in 21 of 36 (58%) given nonirradiated cells. Between 60 and 130 days of age, however, spontaneous diabetes occurred in 18 of 34 untreated control rats (53%) and 16 of 32 rats (50%) given two injections of irradiated con A activated spleen cells. We conclude that irradiation prevents adoptive transfer of BB/W rat diabetes and that irradiated con A activated lymphocytes from acutely diabetic rats do not protect against spontaneous disease in susceptible recipients.

Animals↗
PubMed1976

H-2 restriction of virus-specific T-cell-mediated effector functions in vivo. II. Adoptive transfer of delayed-type hypersensitivity to murine lymphocytic choriomeningits virus is restriced by the K and D region of H-2.

In mice, primary footpad swelling after local infection with lymphocytic choriomeningitis virus (LCMV) and delayed-type hypersensitivity (DTH) adoptively transferred by LCMV immune lymphocytes are T-cell dependent. Nude mice do not develop primary footpad swelling, and T-cell depletion abrogates the capacity to transfer LCMV-specific DTH. Effector T cells involved in eliciting dose-dependent DTH are virus specific in that vaccinia virus-immune lymphocytes could not elicit DTH in LCMV-infected mice. The adoptive transfer of DTH is restricted to H-2K or H-2D compatible donor-recipient combinations. Distinct from the fowl-gamma-globulin DTH model, I-region compatibility is neither necessary nor alone sufficient. Whatever the mechanisms involved in this K- or D-region associated restriction in vivo, it most likely operates at the level of T-cell recognition of "altered self" coded in K or D. T cells associated with the I region (helper T cells and DTH-T cells to fowl-gamma-globulin) are specific for soluble, defined, and inert antigens. T cells associated with the K and D region (T cells cytotoxic in vitro and in vivo for acute LCMV-infected cells, DTH effector T cells, and anti-viral T cells) are specific for infectious, multiplying virus. The fact that T-cell specificity is differentially linked with the I region or with the K and D regions of H-2 may reflect the fundamental biological differences of these antigens. Although it cannot be excluded that separate functional subclasses of T-effector cells could have self-recognizers for different cell surface structures coded in I or K and D, it is more likely that the antigen parameters determine whether T cells are specific for "altered" I or "altered" K- or D-coded structures.

Animals↗
PubMed2000

Temporal relationship between immune cell influx and the expression of inducible nitric oxide synthase, interleukin-4 and interferon-gamma in pancreatic islets of NOD mice following adoptive transfer of diabetic spleen cells.

Beta cell destruction in NOD mice can be accelerated by adoptive transfer of diabetic spleen cells into irradiated adult NOD mice. Here mice receiving diabetic spleen cells were examined at days 0, 7, 14, 21 and at onset of diabetes for the resulting insulitis and the number of intra-islet CD4 and CD8 cells and macrophages. The progression of insulitis and the number of intra-islet CD4 and CD8 cells and macrophages were correlated with the expression and co-localization of inducible nitric oxide synthase, interferon-gamma and interleukin-4 by dual-label light and confocal immunofluorescence microscopy. Diabetes developed in 7/8 mice by 27 days following cell transfer. The insulitis score increased slightly by day 7 but rose sharply at day 14 (p = 0.001) and was maintained until diabetes. The mean number of intra-islet CD4 and CD8 cells and macrophages showed a similar trend to the insulitis scores and were present in almost equal numbers within the islets. Immunolabelling for inducible nitric oxide synthase was observed at day 7 in only some cells of a few islets but increased sharply from day 14. It was restricted to islets with insulitis and was co-localized in selective macrophages. Weak intra-islet interleukin-4 labelling was observed at days 7 and 14 but became more pronounced at day 21 and at onset of diabetes, being present in selective CD4 cells. Intra-islet labelling for interferon-gamma was first observed at day 21, but became more intense at onset of diabetes and was co-localized in a proportion of macrophages. Both cytokines were expressed in islets with advanced insulitis. Interferon-gamma staining was also observed within endothelial cells located in the exocrine pancreas. We conclude that transfer of diabetic spleen cells results in a rapid influx of CD4 and CD8 cells and macrophages within the pancreas of recipient mice. During the period of heightened insulitis, selective immune cells begin to express inducible nitric oxide synthase and the opposing cytokines, interferon-gamma and interleukin-4. Expression of these molecules becomes more pronounced immediately prior to and during the onset of diabetes.

Adoptive Transfer↗
PubMed1984

Murine interstitial nephritis. II. The adoptive transfer of disease with immune T lymphocytes produces a phenotypically complex interstitial lesion.

The present studies demonstrate that immune Thy-1.2+, Lyt-1.2+ T lymphocytes harvested from SJL mice with anti-tubular basement membrane disease can adoptively transfer interstitial nephritis into naive recipients. The lesions produced after cell transfer do not occur immediately but rather take 4 to 6 wk to fully develop. Interstitial lesions can also be transferred to a lesser degree and over a longer period of time with immune serum containing anti-tubular basement membrane antibodies. The fully formed lesions that developed after the transfer of immune cells or serum were phenotypically characterized by cell-surface antibodies using immunofluorescence. T lymphocytes, natural killer cells, macrophages, and Ig+ cells were all well represented in both lesions. Natural killer cells, however, were slightly more prevalent in the lesions of mice receiving immune serum. These experiments demonstrate a potential role for both immune T lymphocytes and anti-tubular basement membrane antibodies in the development of interstitial nephritis in mice. Unlike guinea pigs and rats, it is only in mice that interstitial lesions can be adoptively transferred with immune T lymphocytes, and as such, this model should prove very useful in the additional dissection of cellular interactions and immunoregulatory events that formulate the final effector mechanisms of disease expression.

Animals↗
PubMed1976

Local adoptive transfer of antitumor cellular immunity to xenogeneic animals studied with a rapid radioisotopic footpad assay.

The antitumor cellular immune response to Gross virus-induced rat tumor cells in F344 rats, as measured by a sensitive radioisotopic footpad assay, was adoptively transferred to syngeneic rats and to xenogeneic irradiated BALB/c mice. Xenogeneic transfer was accomplished by the injection of a mixture of rat tumor cells and syngeneic spleen cells, peritoneal exudate cells, or blood lymphocytes from specific immune rats into the footpads of mice. Peritoneal exudate cells produced the strongest footpad reaction in xenogeneic recipients. Use of the xenogeneic adoptive transfer system in a bioassay for human antitumor immunity appeared feasible.

Animals↗
PubMed1994

The infiltration of experimentally induced lung metastases of colon carcinoma CC531 by adoptively transferred interleukin-2-activated natural killer cells in Wag rats.

The number of IL-2-activated natural killer (A-NK) cells reaching the tumor site in vivo may be crucial for their anti-tumor effect following adoptive immunotherapy. We investigated in a syngeneic rat model the infiltration of established lung metastases by adoptively transferred A-NK cells. The Wag rat colon carcinoma CC531 was injected via a tail vein to induce pulmonary metastases. Syngeneic A-NK cells were labeled with the fluorescent dye rhodamine (TRITC) and next injected via a tail vein in rats bearing day-12 lung tumors. The number of A-NK cells in tumor and in normal tissue per rat was counted in sections after administration of A-NK cells. At all time points tested, a significant linear relationship between the cross-section area of the tumor and the number of infiltrating cells was observed, but small tumor areas became fully infiltrated earlier than larger areas. At 24 hr after injection, approximately 10% of the injected cells were found in the tumor tissue and the average A-NK-cell-to-tumor-cell ratio was estimated to be 1:3. A-NK cells were found in the liver too, although the number of cells per mm2 tissue was low compared with the pulmonary tumor tissue. Very low numbers of A-NK cells were found in kidney, adrenal gland, spleen, and blood. We conclude that, in this syngeneic rat model, adoptively transferred A-NK cells are able to find and specifically infiltrate pulmonary metastases in a time-dependent fashion.

Animals↗
PubMed1984

Adoptive transfer of delayed type hypersensitivity reactions specific for Leishmania major antigens to normal mice using murine T cell populations and clones generated in vitro.

Leishmania major specific murine T cell blasts and clones maintained in vitro were tested for their ability to adoptively transfer delayed type hypersensitivity (DTH) reactions to normal mice. These effector cells exhibited a Lyt 1+2- cell surface phenotype. They induced specific DTH reactions in syngeneic DBA/2 mice after local transfer in the footpad, (together with parasite antigens) or intravenous injection followed by challenge with parasite antigens in the footpad. The DTH reactions were specific for L. major antigens and required H-2 identity between the injected T cells (clones) and the adoptively transferred host. Using radioactively labelled T cell blasts for intravenous transfer, it was demonstrated that a large fraction of these functionally active cells localized in the spleen and footpad which had been challenged with parasite antigens.

Animals↗