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PubMed1984

The Lyt phenotype of the T cells in an antitumor adoptive transfer differs for "parent to F1" and "parent to parent" combinations.

The T-cell subset mediating tumor graft neutralization was characterized in a methylcholanthrene (MC) tumor system. Lyt 1+ cells were critical for the successful prevention of outgrowth of the tumor cells in graft neutralization assays with irradiated recipients. Elimination of Lyt 1+ cells abolished the outgrowth inhibitory effect exerted by T-cell-enriched populations derived from syngeneic or semisyngeneic mice immunized with the H-2-carrying MC-induced M-A tumor. In accordance, lymphocyte populations containing 98% Lyt 1+ cells derived from M-A-immune mice, mediated a complete transplantation immunity against this tumor. When the immune T cells admixed to the tumor inoculum were syngeneic to the recipient (i.e., A-derived cells were transferred to A recipients, or F1 to F1), elimination of the Lyt2+ cells did not influence the potential to inhibit tumor outgrowth. The presence of Lyt 1+2- cells were thus necessary, and sufficient, in the syngenic combination. A reduction of the graft-inhibiting potential occurred after elimination of Lyt 2+ cells from the A-derived M-A immune T-cell population when the recipients were semisyngeneic (i.e., (A/Sn X A.SW)F1, (A/Sn X CBA)F1, or (A/Sn X C57B1/6)F1). Consequently, only in the semisyngeneic, but not in the syngeneic combinations, was the transfer of Lyt 2+ cells necessary for optimal graft inhibition. It can be concluded that the genotypic relation between the donor and the recipient influences the prerequisites of the tumor cell neutralization.

Animals↗
PubMed1987

Adoptive transfer of murine autoimmune orchitis to naive recipients with immune lymphocytes.

A protocol was developed for reproducibly transferring experimental autoimmune orchitis (EAO) to naive recipient mice. Cell donors were (C57BL/6 x A/J)F1 mice immunized about 14 days earlier with mouse testicular homogenate with Freund's adjuvant and an extract of Bordetella pertussis. Lymphocytes from lymph nodes and spleens were equally capable of transferring disease. As few as 5 X 10(6) cells were able to transfer EAO, which began on Day 5-7 after transfer. Infiltrate of lymphocytes and macrophages in the region of the rete testis and straight tubules was the most reproducible early lesion, suggesting that this is the initial site of T cell-antigen interaction. It was not necessary to use both Mycobacteria and B. pertussis adjuvants in donor immunization to achieve transfer of EAO. Disease transfer was antigen specific since only cells from donors immunized with TH could transfer disease. In vitro stimulation of the cells with testicular antigens and/or concanavalin A was a prerequisite to successful transfer of EAO, which was dependent on the presence of L3T4+ T cells since depletion of these cells greatly diminished EAO in recipients and the lymphocyte proliferation response to testicular antigens. Disease did not depend on an antibody response by the recipients. The results imply that effector cells, once generated by immunization and fully activated or selected by in vitro stimulation, can home to specific locations in the testis, locate relevant autoantigens, and cause disease.

Adjuvants, Immunologic↗
PubMed1987

Anti-asialo GM1 eliminates both inflammatory process and cytotoxic T-cell function in the lymphocytic choriomeningitis adoptive transfer model.

The induction of severe inflammatory process and fatal neurological disease by transfer of lymphocytic choriomeningitis virus (LCMV)-immune T cells into cyclophosphamide (Cy)-suppressed LCMV-infected mice is greatly inhibited by treatment of these recipients with antibody to the asialo GM1 ganglioside (anti-ASGM1). Examination of cytotoxic activity in lymphoid tissue of the Cy-suppressed recipients at 72 hr after cell transfer revealed that anti-ASGM1 treatment prevented the development of the cytotoxic T lymphocyte (CTL) response, even though the dose of antibody used did not significantly decrease CTL generation in unsuppressed mice. Abrogation of CTL activity was also observed following antibody treatment of NK-deficient (bg/bg) Cy-suppressed recipients, indicating that the anti-ASGM1 was unlikely to be operating via removal of NK cells that are in some way involved in the development of the CTL response. The possibility that anti-ASGM1 may act directly on T cells should be considered in all protocols involving the use of this reagent in immunosuppressed mice.

Animals↗
PubMedDate not supplied

Adoptive transfer of experimental allergic encephalomyelitis from immature guinea pig donors.

In immature Strain 13 guinea pigs sensitized to syngeneic spinal cord, a chronic allergic encephalomyelitis is elicited reminiscent of demyelinating diseases of man and which features relapses or progressive downhill course and extensive areas of demyelination in the central nervous system. However, juvenile recipients of syngeneic lymphocytes from similarly sensitized juveniles show only the acute form of experimental allergic encephalomyelitis. Neuropathologically, the CNS of affected animals displayed mild changes only and minimal demyelination. These observations indicate that the age-dependent differences seen between the acute disease of adults and the chronic disease of juveniles may be due to differences in availability of modulating or reparatory factors, rather than differences in the central nervous system organ or in the immune response itself.

Acute Disease↗
PubMed1986

Adoptive transfer of experimental allergic encephalomyelitis with lectin-activated spleen cells. Part 2. Studies on T cell subsets and interleukin 2 production.

Experimental allergic encephalomyelitis (EAE) can be transferred by spleen cells stimulated in vitro with D-mannose-binding lectins but not with N-acetyl-D-galactosamine (GalNAc)-binding lectins. EAE could also be passively transferred by spleen cells following incubation with wheat germ agglutinin (WGA), in which case the disease transfer was abolished by the specific hapten inhibitor, N-acetyl-D-glucosamine. In the presence of rat T cell monoclonal antibody, either W3/25 or OX-8, both concanavalin A and Wisteria floribunda agglutinin stimulated helper and suppressor T subpopulations. On the other hand, GalNAc-binding lectins were less effective than D-mannose-binding lectins in generating interleukin 2 (IL2) in the culture supernatant, whereas WGA-stimulated spleen cells did not produce IL2. Furthermore, spleen cells cultured with pure IL2 could not transfer EAE to the recipients. These data suggest that some factors distinct from IL2 are required for the differentiation of EAE-effector precursors into the final effector cells in this transfer system.

Animals↗
PubMed1984

Adoptive transfer of suppression of experimental allergic orchitis with lymphoid cells from antigen-pretreated guinea pigs.

The injection of lymph node cells or spleen cells, obtained from strain 13 guinea pigs rendered unresponsive to experimental allergic orchitis (EAO) by pretreatment with testicular antigen (TA) in incomplete Freund's adjuvant, into normal syngeneic recipients markedly prevented the development of EAO, especially of the interstitial inflammatory cell response, which was expected to occur 2 weeks following orchitogenic challenge with TA in complete Freund's adjuvant (CFA). The suppressive effect of thymus cells from the same donors was much less prominent. The inhibition of EAO by suppressor cells was specific for the relevant antigen TA. In such EAO-suppressed animals delayed skin reaction to TA was suppressed, whereas antisperm antibody formation was not impaired. The active suppressor cells residing in the lymph nodes had characteristics of T lymphocytes, in that they did not adhere to the plastic dish surface and nylon wool and in that they formed rosettes with rabbit erythrocytes. B lymphocytes from the same animals did not have detectable suppressive properties. Lymph node cells from protected donors that had been treated with a single dose of cyclophosphamide (CY) 3 days before cell transfer were unable to transfer unresponsiveness to EAO. The results suggest that the immune prevention against EAO is explainable at least in part by the generation of CY-sensitive suppressor T lymphocytes with the capacity of inhibiting development of effector T cells after antigenic stimulation and that suppressor cells that mediated unresponsiveness to EAO may also regulate the cellular hypersensitivity to TA.

Animals↗
PubMed1984

Antigen-specific suppression of collagen arthritis by adoptive transfer of spleen cells.

Wistar-Furth (W-F) rats were given 10(9) syngeneic spleen cells, suspended in Hanks' balanced salt solution (HBSS), intravenously on Day 0 to investigate the mechanisms involved in antigen-specific suppression of collagen arthritis. These cells were pooled from W-F donors which had been injected iv on Days -21, -14, and -7 with rat red blood cells (RBC) coupled with glutaraldehyde to either native chick type II collagen, denatured type II collagen, or native type I collagen. All recipients were immunized with an emulsion of native type II collagen in incomplete Freund's adjuvant on Day 1 to induce collagen arthritis. There was a decreased incidence of arthritis, by clinical and radiographic assessments, in rats receiving spleen cells from donors previously administered native type II collagen-coupled RBC compared to those given spleen cells obtained from donors treated with denatured type II or native type I collagen-coupled RBC [18 of 30 (60%) arthritic vs 20 of 20 (100%) and 19 of 20 (95%) arthritic, for the three groups, respectively, P less than 0.01 for both comparisons]. The incidence of arthritis in 35 rats administered HBSS iv 1 day prior to immunization (83%) and 10 immunized rats given no iv injections (100%) was also significantly higher (P less than 0.05) than the incidence in the antigen-relevant experimental group. Hemagglutinating antibody titers and delayed-type hypersensitivity (DTH) to collagen were lower in the recipients of cells from donors administered native type II collagen-coupled RBC, whereas IgG antibody titers to collagen were unaltered. These results demonstrate that passively transferred spleen cells can attenuate collagen arthritis and sensitization in an antigen-specific manner.

Animals↗
PubMed1988

Role of Ia antigen in the induction of adoptively transferred acute and chronic relapsing demyelinating disease in mice.

Acute and chronic relapsing forms of experimental allergic encephalomyelitis (EAE) can be induced in SJL/J mice following transfer of myelin basic protein (MBP)-sensitized T cells which have been challenged in vitro with MBP. In this study, addition of specific anti I-A antibody during the culture blocked the antigen-specific proliferation of T cells and inhibited the transfer of both acute and relapsing EAE. Treatment of T cell recipients with anti I-As antibody daily for 10 days suppressed the induction of acute EAE. Further treatment of mice with anti I-As antibody reduced the number of relapses and improved their conditions. We conclude that MBP-sensitized T cells interact with Ia positive cells, both in vitro and in vivo, to induce acute and chronic relapsing EAE, respectively. The mechanism of this interaction and its role in the disease process are discussed.

Acute Disease↗
PubMed1984

Immunity to Babesia in mice. I. Adoptive transfer of immunity to Babesia rodhaini with immune spleen cells and the effect of irradiation on the protection of immune mice.

Immunisation of Balb/c mice against Babesia rodhaini by an amicarbalide-controlled infection resulted in a solid immunity which lasted for 216 days. With spleen cells of immune mice protection could be transferred both to naive mice pretreated with cyclophosphamide. Treatment of naive mice with cyclophosphamide (300 mg/kg) five days before a lethal B. rodhaini inoculation resulted in over 50% survival. This protective effect of cyclophosphamide is explained by its inhibiting effect on suppressor T-cells. The protection against B. rodhaini challenge infection afforded to immune Balb/c mice was completely resistant to a sublethal irradiation of 400 rad. Since B-lymphocyte function in antibody production is suppressed by this dose, the role of antibodies in the effector phase of the immunity appears to be of minor if any importance. A considerable degree of protection was still preserved after irradiation of immune animals with 875 rad. Sensitivity to this irradiation dose of all immunocompetent cells except macrophages and a small fraction of T-lymphocytes indicates the involvement of these cell types in the effector phase of the specific immunity. Highly radioresistant macrophages are therefore considered to play the major role but T-lymphocytes are also required for complete protection.

Animals↗
PubMed1987

Adoptive transfer of suppression of the autoimmune response to rat male accessory glands: characterization of the suppressor cells.

We have examined the mechanism of suppression of autoimmunity to rat male accessory glands (RAG) by T suppressor cells. This suppression was accomplished by transfer to syngeneic rats of spleen mononuclear (SpM) cells from rats rendered unresponsive by pretreatment with low doses of a purified fraction of RAG (containing the autoantigen). The experiments demonstrated that the suppressor cells that act on the inducer phase of the suppression are cyclophosphamide (Cy) sensitive and that they can be positively selected on antigen-coated plates. On the other hand, the inducer phase T suppressor cells present on spleens coming from antigen-pretreated rats did not suppress the autoimmune response in normal recipients that had been irradiated (850 rad 137Cs) just prior to receiving the cells or injected with Cy 14 days after transfer. The results indicate that the regulation of immune response to the autoantigen of RAG is complex and that it involves the interaction of many cell types.

Animals↗
PubMed1989

The adoptive transfer of chronic relapsing experimental allergic encephalomyelitis with lymph node cells sensitized to myelin proteolipid protein.

In this report we describe the transfer of chronic relapsing experimental allergic encephalomyelitis (EAE) with in vitro-stimulated lymph node cells (LNC) from SJL/J mice immunized with human myelin proteolipid protein (PLP). No additional immune enhancing procedures were applied in the transfer recipients. Clinical and histological EAE was transferred with 10-30 X 10(6) LNC to 27/28 mice. The LNC proliferated in vitro to PLP, but not to myelin basic protein (MBP), and induced delayed-type hypersensitivity. Enrichment for lymphoblasts by Ficoll centrifugation was essential for the disease development. The clinical course usually showed an early episode of acute paralytic illness, followed by chronic relapsing disease, and resembled the transfer of EAE using MBP-specific cells, both clinically and histologically.

Animals↗