Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADOPTION”

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 1,729 records · Page 96Linked to original sources

Adoptive protection against Plasmodium chabaudi adami malaria in athymic nude mice by a cloned T cell line.

T cell-dependent, cell-mediated immune mechanisms have been shown to contribute to resistance against malaria. Because the identity of plasmodial Ag responsible for the activation of these protective immune responses remains unknown, a major step in isolating these potential immunizing agents will be the development of adequate screening procedures designed to identify important T cell Ag. This study focused on the isolation of protective T cell clones that may play a pivotal role in this process. A T cell clone designated CTR2.1 and two subclones derived from it adoptively transferred protection to athymic nude mice infected with Plasmodium chabaudi adami, a murine malarial parasite known to be recognized by protective thymus-dependent immune mechanisms. The protective T cell clone displayed a L3T4+, Lyt-2- surface phenotype and secreted both IFN-gamma and IL-2 after stimulation with solubilized parasites in vitro. This is the first report of results demonstrating a cloned T cell line capable of providing adoptive protection against malaria in vivo. More importantly, CTR2.1 and other protective T cell clones may provide for the identification of plasmodial antigenic epitopes recognized by important cell-mediated immune mechanisms during acute malarial infection.

Animals↗

Adoptive immunotherapy of syngeneic murine leukemia is enhanced by the combination of recombinant IFN-gamma and a tumor-specific cytotoxic T cell clone.

Mice with an established syngeneic T cell tumor (RBL5) received short term adoptive chemoimmunotherapy with CTL clone 1.B6 and murine rIFN-gamma. In comparison with treatment with either agent alone, the combination of 1.B6 and rIFN-gamma was associated with a dramatic increase in long term survival. No direct effects of rIFN-gamma on tumor cell proliferation, MHC Ag expression, or susceptibility to CTL-mediated lysis could be demonstrated to explain the prolongation of survival. However, rIFN-gamma induced a distinct increase in broad-spectrum cytolytic capacity of peritoneal exudate cells and further increased class II MHC expression on peritoneal macrophages. The explanation for enhanced adoptive chemoimmunotherapy after combined short term administration of a CTL clone and rIFN-gamma is uncertain. Potential mechanisms include direct tumor lysis by activated cells, indirect tumor lysis via sensitization to other lymphokines or monokines, improved Ag-specific activation of transferred CTL clones, and/or more effective development of de novo host anti-tumor immunity.

Animals↗

Selective idiotype suppression of an adoptive secondary antiacetylcholine receptor antibody response by immunotoxin treatment before transfer.

Acetylcholine receptor (AChR)-immune lymph node cells were treated with Id-specific immunotoxin before their transfer and antigenic challenge in adoptive recipient rats. In contrast to untreated, AChR-immune lymph node cells that, when challenged, produced high titers of serum anti-AChR antibody, in vitro anti-Id-ricin A chain treatment significantly inhibited anti-AChR antibody responses upon adoptive transfer. The inhibition was specific in that control lymph node cells immune to keyhole limpet hemocyanin were unaffected and totally responsive after treatment by the same immunotoxin. Furthermore, evidence is presented by isoelectric focusing analysis that the anti-Id antibody preparation used in this study contains all of the specificities required to eliminate the entire spectrum of AChR-reactive B cell clones.

Acetylcholine↗

Cellular basis of immunologic interactions in adoptive T cell therapy of established metastases from a syngeneic murine sarcoma.

The adoptive transfer of specifically sensitized T lymphocytes can effectively mediate the regression of established local and metastatic tumors. Previous experiments using the weakly immunogenic MCA 105 sarcoma indicated that cellular interactions between transferred L3T4+ helper and Lyt-2+ cytotoxic immune T cells were necessary for mediating tumor regression. In this study, the kinetics of T-T cell interactions were analyzed by in vivo depletion of T cell subsets with mAb. The anti-tumor efficacy of transferred immune cells was abrogated by in vivo administration of either L3T4 or Lyt-2 mAb on the day of cellular therapy. However, if mAb were given 3 days after the transfer of immune cells, depletion of Lyt-2+ but not L3T4+ cells abrogated anti-tumor efficacy. T cell depletion on day 6 after transfer of immune cells had no adverse effect on tumor regression, indicating the period required for T cell reactivity in vivo. Furthermore, depletion of Ia+ cells by in vivo mAb treatment abrogated the anti-tumor efficacy of immune cells. It is thus hypothesized that there are two distinct but sequential phases of in vivo T cell interactions leading to the regression of established tumors after adoptive immunotherapy. An initial "helper/inducer" phase apparently requires the interaction of L3T4+ immune cells and the tumor Ag involving Ia+ cells. The inducement of L3T4+ cell activation is to provide helper function via the secretion of IL-2. The second phase designated as an "effector phase" involves differentiation of immune Lyt-2+ cells under the influence of IL-2 secreted during the helper/inducer phase for generation of mature Lyt-2+ effector cells. To further support the hypothesis of a two-phase process we have examined the phenotype and kinetics of tumor regression mediated by effector cells generated by secondary in vitro sensitization (IVS). Although the IVS cells were generated from fresh MCA 105 immune spleen cells, their anti-tumor efficacy was mediated solely by Lyt-2+ lymphocytes. Kinetic studies revealed that the in vivo requirement of IVS Lyt-2+ effector cells to mediate tumor regression was less than 3 days, and the anti-tumor reactivity of these cells was not affected by in vivo depletion of Ia+ cells. Thus, the IVS reaction is likely representative of the in vivo counterpart of the helper/inducer phase leading to the generation of mature Lyt-2+ immune effector cells. Tumor regression after transfer of Lyt-2+ cells generated in IVS therefore required a relatively shorter period of time than that required after the transfer of fresh noncultured MCA 105 immune spleen cells.

Animals↗

Adoptive immunotherapy of human cancer using low-dose recombinant interleukin 2 and lymphokine-activated killer cells.

The adoptive transfer of recombinant-methionyl human interleukin 2 (rIL-2)-activated autologous peripheral blood mononuclear lymphokine-activated killer (LAK) cells to cancer patients is being evaluated as an alternative to conventional cancer therapy. We have independently developed an alternative regimen to previously reported adoptive immunotherapy protocols using rIL-2 and LAK cells which features the prolonged administration of low-dose rIL-2 (30,000 units/kg) and an automated, entirely enclosed system of peripheral blood cell procurement, culture, harvest, and reinfusion of activated cells. The cell culture system was tested with a murine tumor model in which LAK cells generated in plastic culture bags were reinfused into tumor-bearing mice. Tumor regression was as effective with cells activated in the bags as in conventional culture flasks. Twenty-eight cancer patients were treated for 5 consecutive days with low-dose rIL-2, followed by leukapheresis, infusion of LAK cells, and prolonged IL-2 administration. At least 50% tumor regression was observed in 46% of all patients treated. These data imply that human peripheral blood mononuclear cells retain fully their capacity for rIL-2-induced activation and effector cell function under this alternative approach, and further, that a low-dose rIL-2 regimen with markedly reduced toxicities can be as effective as high-dose rIL-2 regimens if low-dose rIL-2 is given for a prolonged period of time following LAK cell infusion.

Adult↗

Adoptively transferred reactivity to M. leprae in nude mice infected with M. leprae.

Reversal reactions are manifestations of delayed hypersensitivity to M. leprae and are thought to be usually accompanied by manifestations of effective cell-mediated immunity (CMI) as measured by bacterial clearing. These experiments were designed to study the induction of reversal reactions in M. leprae-infected, congenitally athymic nude mice using adoptive transfer of CMI. Splenic cell suspensions derived from unimmunized heterozygous nu/+ mice, and those vaccinated with heat-killed M. leprae, viable BCG and a mixture of the two antigens were diluted to contain 10(4), 10(5), 10(6), 10(7) lymphocytes/0.1 ml and infused intravenously into multibacillary nude mice. The production of reversal reactions in leprous nude mice in response to adoptively transferred CMI was studied in a quantitative fashion. Dose responsive induction of reversal reactions, apparent by footpad inflammation and swelling, decreased morphological indices (MI) of the bacteria and mononuclear cell infiltrations, histopathologically, were observed. For nude mice receiving cells primed with 3.9 X 10(5) living BCG alone, the effective dose 50% (ED50) was 1.0 x 10(6) lymphocytes to induce reversal reactions. For those receiving cells primed with 10(7) M. leprae the ED50 was 3.7 x 10(5) lymphocytes. For nude mice receiving cells primed with a mixture consisting of 1/2 the above dose of BCG + 1/2 the above dose of M. leprae, the ED50 was 6.8 x 10(4) lymphocytes.

Animals↗

[Clinical studies of adoptive immunotherapy of human disseminated brain tumors with LAK cells and recombinant interleukin-2].

In previous in vitro studies, the authors showed that recombinant interleukin-2 (rIL-2) stimulated peripheral blood lymphocytes (PBL) from patients with malignant brain tumors to generate cells that were lytic for fresh autologous tumor but not for lymphocytes or lymphoblasts. We then tried the adoptive transfer of such lymphokine-activated killer-(LAK) cells induced from patients with meningeal gliomatosis (MG) and meningeal carcinomatosis (MC). PBL fractions were separated into a plastic bag by leukophoreses using HEMONETICS V 50. PBL were then harvested by LSM (Litton Bionetics, Kensington, Md.) gradient centrifugation according to the standard method. Human LAK cells were generated by placing 5 X 10(7) PBL in 10-cm diameter plastic dishes (Falcon) holding 20 ml of complete medium (CM) containing 100 units of rIL-2 (TGP-3, provided by TAKEDA Chemical Industries, Ltd.). The CM consisted of RPMI P640 with 0.1 mM nonessential amino acids, 1 microM sodium pyruvate, 5 X 10(-5) M 2-mercaptoethanol, 50 micrograms/ml of gentamicin sulfate, 0.03% glutamine and 2% heat-inactivated human AB serum. The dishes were incubated horizontally at 37 degrees C in a 5% CO2 atmosphere for 72-96 hours. The LAK cells were then harvested, washed three times with Hanks' balanced salt solution (HBSS) and resuspended in HBSS for transfer to patients. 1-2 X 10(8) LAK cells were injected intrathecally through Ommaya's reservoir or a V-P shunt reservoir twice a week. Portions of LAK cells were tested for cytotoxicity in vitro. During the adoptive transfer of LAK cells, patients were given intravenous injections of 500 units of rIL-2 every day. Case 1: A 29-year-old man with meningeal gliomatosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Adoptive immunotherapy of cancer patients with lymphokine-activated killer cells].

We have examined the effects of recombinant human interleukin-2 (rIL-2) on generation of lymphokine-activated killer (LAK) cells and adoptive immunotherapy. rIL-2 generated LAK activity dose- and time-dependently. The generated LAK cells by rIL-2 killed autologous and various allogenic tumor cells but not normal cells. No difference was found in the generation of LAK activity by rIL-2 between healthy donors and cancer patients rIL-2 generated LAK activity of lymphocytes obtained from peripheral blood, spleen, pleural fluid and ascites in cancer patients. Two cancer patients with pleuritis carcinomatosa, who had not responded to various chemotherapeutic agents, were treated with adoptive immunotherapy. LAK cells were generated from the lymphocytes of pleural fluid or peripheral blood incubated with rIL-2 (5 U/ml) for 5 days. LAK cells (0.1-1.0 X 10(9)/100 ml in total) were administered into the pleural cavity followed by injection of rIL-2 (1,000 U) 1 to 7 times. No significant adverse effect was observed except for fever and eosinophilia. Complete disappearance of pleural tumor cells was observed in one patient and decrease in the other.

Aged↗

[Lymphokine-activated killer (LAK) adoptive immunotherapy: optimal method for large-scale LAK induction].

Adoptive immunotherapy with lymphokine-activated killer (LAK) cells shows promise as a treatment for malignant disease, but one of the difficult problems associated with the LAK therapy is the method to induce 10(11) to 10(12) of LAK cells. In a study for optimal LAK induction, monocytes separated with counterflow centrifugal elutriation markedly augmented LAK cell induction from lymphocytes in spite of having no cytotoxicity when cultured alone; LAK activity was sufficiently induced from mononuclear cells (MNC) containing approximately 20% of monocytes; LAK activity was induced depending on the serum concentration, and at least 5% of human AB serum in RPMI 1640 was referred to induce optimal LAK activity; and roller bottle was preferable to tube or flask especially at higher MNC density. We concluded that roller bottle with 4 X 10(6) cells/ml of MNC suspended in 1 liter of RPMI 1640 containing 5% AB serum would be the optimal condition for large-scale LAK induction, and administration of LAK cells on the 3rd and 4th day of culture is favorable for weekly performance of LAK adoptive therapy.

Cell Separation↗

Severe hypovitaminosis C occurring as the result of adoptive immunotherapy with high-dose interleukin 2 and lymphokine-activated killer cells.

Adoptive immunotherapy of human cancer was investigated in our institution as part of a National Cancer Institute extramural group study. This treatment, for patients with metastatic malignant melanoma, hypernephroma, and colon carcinoma, consisted of three phases: (a) 5 days of i.v. high-dose (10(5) units/kg every 8 h) interleukin 2, (b) 6 1/2 days of rest plus leukapheresis; and (c) 4 days of high-dose interleukin 2 plus three infusions of autologous lymphokine-activated killer cells. Toxicities included fever, chills, tachycardia, hypotension, vomiting, diarrhea, and fluid retention. Ascorbic acid is known to be important to cell-mediated immunity, and it has been reported to be depleted during physiologically stressful events. Therefore, we determined plasma ascorbic acid levels in patients (n = 11) before adoptive immunotherapy and before and after Phases 1, 2, and 3 of treatment. Patients entering the trial were not malnourished. Mean plasma ascorbic acid levels were normal (0.64 +/- 0.25 mg/dl) before therapy. Mean levels dropped by 80% after the first phase of treatment with high-dose interleukin 2 alone (0.13 +/- 0.08 mg/dl). Mean plasma ascorbic acid levels remained severely depleted (0.08 to 0.13 mg/dl) throughout the remainder of the treatment, becoming undetectable (less than 0.05 mg/dl) in eight of 11 patients during this time. Values obtained from 24-h urine collections on two of two patients indicated that ascorbate was not excreted in the urine. Plasma ascorbic acid normalized in three of three patients tested 1 mo after the completion of treatment. Unlike the results for ascorbic acid, blood pantothenate and plasma vitamin E remained within normal limits in all 11 patients throughout the phases of therapy. Responders (n = 3) differed from nonresponders (n = 8) in that plasma ascorbate levels in the former recovered to at least 0.1 mg/dl (frank clinical scurvy) during Phases 2 and 3, whereas levels in the latter fell below this level.

Adult↗

[Correlation between the anti-arrhythmia effect of ethacizin and pharmacokinetic parameters in a model of rhythm adoption by the heart].

Pharmacokinetics and pharmacodynamics of ethacizin were studied in a model of rhythm adoption by the heart, with the drug administered intravenously to anesthetized cats. A relation was demonstrated between blood ethacizin pattern and the drug's biphasic effect on the adoption of stimulation-imposed pace by the heart and ventricular fibrillation threshold. The estimated correlation coefficients, reflecting the relationship between the development of ethacizin anti-arrhythmic and antifibrillation effects and variation of its plasma levels between 10 and 120 min after the administration, were rather high (-0.85 and +0.93, respectively). Ethacizin shows anti-arrhythmic and antifibrillation activity when its plasma levels are between 2400 and 200 ng/ml.

Animals↗

[Immunologic memory for Staphylococcus studied by adoptive transfer].

The basic regularities of the formation and realization of immunological memory to staphylococcal corpuscular antigen were studied in adoptive transfer experiments on CBA mice. The capacity of spleen cells for generating anamnestic response to staphylococci in the body of irradiated syngeneic recipients appeared on day 3 after the immunization of donors. The formation of immunological memory to staphylococci in mice was shown to be directly related to the dose of the antigen. The study also revealed that intact splenocytes did not suppress the realization of immunological memory to staphylococci in the system of adoptive transfer. The conclusion of the absence of the "isogeneic barrier" for memory cells specific to staphylococcal corpuscular antigen was made.

Animals↗

Curative intravenous adoptive immunotherapy of Meth A murine sarcoma. A histologic and immunohistochemical assessment.

Intravenous administration of 1.5 X 10(8) syngeneic spleen cells from immune animals resulted in the complete eradication of established Meth A soft tissue sarcomas in (C57BL/6 X BALB/c) F1 mice. In mice receiving a single injection of immune spleen cells 4 days after tumor implantation in the abdominal wall, the tumors continued to grow for approximately 1 week before undergoing regression. This delay before adoptive immunity is expressed is thought to represent the time needed for the passively transferred cells to give rise to a host response of sufficient magnitude to destroy the tumor. None of the mice receiving a similar number of control spleen cells were cured of their sarcomas. Successful therapy was dependent upon the transfer of viable, immune T lymphocytes and required prior irradiation of the tumor-bearing host in order to remove suppressor T cells. Utilizing sequential histologic and immunohistochemical techniques, we attempted to characterize the cellular events of tumor regression. The earliest histologic difference between animals treated with immune and nonimmune lymphocytes was in the number of lymphocytes detected at the perimeter of the tumor in specifically immunized mice on day 6. There was also a striking difference between animals treated with immune versus nonimmune lymphocytes in the intensity and timing of the acute inflammatory response beginning on day 8. The "front" of immunologically mediated tumor destruction appeared at the lateral and deep borders of the implanted sarcomas and progressed inward. During the period of active tumor regression T lymphocytes reactive with a biotinylated mouse anti-Thy 1.2 monoclonal antibody were increased in frozen sections of tumors in mice receiving immune cells relative to the controls. During the first 3 weeks following adoptive transfer of lymphocytes, T cells reactive with Lyt-1 biotinylated mouse monoclonal antibody (helper/inducer phenotype) outnumbered their Lyt-2 (suppressor/cytotoxic) counterparts in frozen sections of tumor from both specifically immunized and control mice. By the end of the 4th week of the experiment, the sarcomas were completely eradicated in all mice receiving immune cells. The previous tumor beds were occupied by collections of lipid-laden macrophages, lymphocytes, plasma cells, and fibroblasts. Despite vigorous but delayed acute and chronic inflammatory responses at the tumor perimeters in the control mice, these tumors all progressed.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

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↗

[Study of anti-tetanus immunity in samples of the Italian population. I. Epidemiological considerations on tetanus in Italy and description of the technic adopted for sero-epidemiological studies].

The effectiveness of vaccinal prophilactic measures adopted in Italy since 1963 both on a volluteer and on a compulsory base, is analyzed according to the specific morbidity rates computed on a national base up to 1973. Rates for infants and young people have dramatically decreased, but rates for adult and old subjects still keep unmodified. Therefore, a tetanus vaccination involving adults and old people seems advisable, followed, as for children, by regular booster injection. A study on levels of immunity in samples of the population and another study on the duration of immunity after vaccination are supposed to be a reasonable base on which to build a program of vaccination in adults and old people. Such studies will be detailed in Note II and Note III. Note I describes and omments the technique adopted for the seroepidemiological studies.

Adolescent↗

Reaginic antibody formation in the mouse. V. Adoptive antihapten IgE antibody response of dinitrophenyl-keyhole limpet hemocyanin-primed spleen cells cultured with dinitrophenyl heterologous carrier conjugates.

DBA/1 mice were primed with dinitrophenyl-keyhole lympet hemocyanin (DNP-KLH) included in aluminum hydroxide gel, and the adoptive anti-DNP IgE antibody response of their spleen cells was studied by transfer into irradiated syngeneic mice. As expected, depletion of T cells by anti-theta antiserum and complement abolished the response of the spleen cells to homologous antigen. If the same T-depleted spleen cells were cultured with DNP-KLH for 24 hr and then transferred into irradiated mice, anti-DNP IgE antibody response was obtained. It was also found that DNP-KLH-primed spleen cells were triggered for IgE antibody response if they were cultured for 24 to 48 hr with DNP heterologous carrier conjugate, such as DNP-bovine gamma-globulin or a copolymer of D-tyrosine, glutamine, and lysine. Transfer of the cells cultured with the antigen into irradiated recipients resulted in the formation of anti-DNP IgE antibody. The DNP-KLH-primed cells cultured for 24 hr in the absence of antigen and then treated with DNP-BGG at 0 degrees C, also gave an adoptive IgE antibody response. If the same DNP-KLH-primed cells were treated with the DNP heterologous carrier conjugate at 0 degrees C or injected into irradiated recipients together with the antigen, no IgE antibody response was obtained. The results indicated that T cell dependency of the IgE antibody response is diminished by culture of DNP-KLH-primed cell for 24 to 48 hr.

Animals↗

Adoptive immunotherapy and chemo-immunotherapy in murine L-1210 leukemia and its influence on the kinetics of leukemic proliferation.

Donor allogeneic C57Bl/6 lymphoid cells from peritoneal cavity, lymph nodes, thymus and spleen of immunized and non-immunized mice were used for adoptive immunotherapy of L-1210 ascites leukemia in DBA/2J recipients. Donor effector cells were injected i.p. into leukemic mice which were given a whole-body irradiation in a dose of 300 r X-rays prior to leukemia inoculation. The in vitro cytotoxicity of the effector cells was tested by the LT- and 51Cr-tests. Cytokinetics of leukemia undergoing therapy was followed by impulse-cytophotometry. An adoptive chemo-immunotherapy with the aid of peritoneal or splenic lymphoid cells from immunized donors proved to be most effective. The cells were injected on the second day into recipients inoculated with leukemia on the day 0, and then given on the first day a single i.p. injection of cyclophosphamide in a dose of 50 mg/kg body weight. Under these conditions the secondary disease did not influence therapy and apart from a distinctly prolonged survival there was also noted a number of permanent survivals of leukemia. It was also found that peritoneal and splenic lymphoid cells of immunized donors exhibited most pronounced direct and indirect cytotoxicity against target cells in vitro. In vivo, the effector cells mounted an attack on the L-1210 cells probably at the onset of the G1-phase of the cell cycle.

Animals↗

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↗