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At least 19 recordsLinked to original sources
PubMed1976

Immune responsiveness and incidence of reticulum cell sarcoma in long-term syngeneic radiation chimeras.

Long-term syngeneic radiation chimeras displayed a very low incidence of reticulum cell sarcoma as compared with control mice. Immune reactivity of these animals was studied in vivo by anti-dinitrophenyl antibody titer and affinity and in vitro by mitotic responsiveness to phytohemagglutinin, concanavalin A and lipopolysaccharide. Anti-body titer and affinity as well as the response to T lectins were found to be increased in chimeras. These results were attributed to increased function of mature T2 cells, which could explain the reduced incidence of reticulum cell sarcoma in chimeras.

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PubMed1976

[Histogenesis of sarcomas, induced by plastic films, in murine radiation chimeras].

Sarcomas were induced in radiation chimeras CBA/CBAT6T6 by subcutaneous implantation of plastic films 13 months after the irradiation and donor bone marrow transplantation. Of the 12 tumours examined, 11 possessed host kariotype and one--donor karyotype. Development of connective tissue cells from the bone marrow precursors presumably played no significant role in the histogenesis of plastic sarcomas.

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PubMed1976

Infusion of donor lymphocytes into stable canine radiation chimeras: implications for mechanism of transplantation tolerance.

Canine radiation chimeras were used to investigate further mechanism(s) responsible for maintaining the stable chimeric state. Chimeras were studied 7 to 46 months after 1200 R total body irradiation and transplantation of marrow from a littermate donor matched at the major histocompatibility complex. An attempt was made to perturb the stable chimeric state by infusion of large numbers (0.6 to 13.7 x 10(8)/kg) of donor peripheral blood lymphocytes into each respective chimera. Two groups were studied: donors in Group A were normal; donors in Group B had been specifically sensitized against minor histocompatibility antigens of the chimera by repeated skin grafts. None of the nine chimeras in Group A developed significant clinical or histologic evidence of graft-vs-host disease (GVHD) after donor lymphocyte infusion. Eight of the 12 chimeras in Group B, however, developed GVHD which was transient in three and fatal in five. The results in Group A are not consistent with classical theories of tolerance, i.e., elimination or inactivation of potentially reactive cell clones, but suggest the presence of an active mechanism suppressing recognition of host antigens by the infused donor lymphocytes and development of GVHD. The results in Group B indicate that this mechanism can be overcome by infusion of sensitized donor cells. In an attempt to elucidate the nature of this postulated active mechanism, the cytotoxicity of donor lymphocytes for fibroblasts of the chimera and the presence or absence of serum-blocking factors were assessed in vitro by using a cellular inhibition (CI) assay. The presence of serum-blocking factors did not protect against the development of significant GVHD in two chimeras (fatal in one). GVHD did not occur in four other chimeras after infusion of cytotoxic donor lymphocytes despite the absence of serum-blocking factors. These and previous results suggest that serum-blocking factors are not the mechanisms suppressing the development of GVHD in canine radiation chimeras, and raise the possibility that a suppressor cell population may be responsible for preventing GVHD.

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PubMed1977

Immune competence of splenic lymphocytes following graft-vs-host disease in mouse allogeneic radiation chimeras.

The abnormal immune response of long-term mouse allogeneic chimeras is reflected by qualitative deficiencies in either T or B lymphocytes. The present study was undertaken to determine if a relationship existed between the severity of graft-vs-host disease (GVHD) that these animals had experienced and a functional defect in either the T or B cell population. The in vitro PFC response of chimera spleen cells to sheep red blood cells (SRBC) was evaluated in the presence of normal T or B lymphocytes 4 to 8 months after marrow transplantation and well beyond the GVHD period. In an analysis of several different allogeneic radiation chimeras, our results showed no relationship between the severity of GVHD experienced and the immunologic capacity of either T or B cells. Thus, different chimera combinations showing similar degrees of GVHD were functionally deficient in one or the other of these two cells types or both with no apparent predilection for abnormality in either population. In examining the quantitative in vitro PFC response to sheep RBC by spleen cells from individual chimeras, we found that the number of PFC formed was related to the severity of GVHD experienced by that animal. A general relationship between severity of GVHD and PFC capacity may also exist between chimeras of different genetic combinations. However, this relationship is not precise since gross exceptions occur. Our results, although documenting further the qualitative abnormalities in T and/or B lymphocytes of radiation chimeras, do not reveal the factor or mechanisms by which these cells are made unresponsive. It is suggested that the tolerance-inducing mechanism of these animals, whether it be humoral blocking factors or suppressor cells, is in some way interfering with the collaboration of T and B cells for antibody production.

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PubMed1976

Reconstitution capacity of bone marrow cells from nude mice in radiation chimeras.

Lethally irradiated mice were reconstituted with bone marrow cells from 'nude' or normal mice. It was found that the radioprotective capacity of bone marrow cells from normal and thymusless 'nude' mice is similar and that the immune responses to sheep red cells in radiation chimeras reconstituted with normal and nude bone marrow cells are also similar. Bone marrow cells from nude mice, in spite of the lack of the thymus, develop into hematopoietic cells and contain also T-precursor cells.

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PubMed1977

[Kinetics of the basic sections of the hemopoietic system in radiation chimeras].

During first 3 days after mice irradiation and syngeneic bone marrow transplantation in them the number of CFUs (about 0,5% of the injected cells) was stable, although the proliferation induction began 24 hours after transplantation. As it was shown by the method of "thymidine self-distruction". Twenty four hours later all the CFUs entered the mitotic cycle. On the contrary, the commited cells (granulopoesis precursors) compartment (CFUc) enters the logarithmic growth phase since the first day. The exponential growth of the CFUs number was observed from the 4th day simultaneously with the increasing of the proliferation rate of CFUc and the beginning of the recovery of the bone marrow cells total number. In late radiation chimeras (1 month after radiation and reconstitution) the total number of CFUs was 50--70% of the initial. The other hemopoetic parameters were in the normal limits.

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PubMed1975

Histocompatibility and T-B cell cooperation in mouse radiation chimeras.

Cooperative interaction between histocompatible as well as histoincompatible T and B cells in vivo was studied with B cell-bearing syngeneic radiation chimeras receiving syngeneic, semiallogeneic, or allogeneic A and T cells in various combinations. The results indicated the following: i) Histoincompatible T and B cells normally did not cooperate successfully for generation of antibody-forming cells. ii) Semiallogeneic (C3BF1) T cells cooperated successfully with parent-type (C3H) B cells developed in parent-type syngeneic chimeras (C3H/C3H), whereas parent-type (C3H as well as C57BL) T cells failed to cooperate with F1 (BC3F1) B cells developed in F1 syngeneic chimeras (BC3F1/BC3F1). iii) T cells obtained from C57BL/C3H or C57BL/C3BF1 chimeras, which were most likely donor (C57BL)- derived, cooperated successfully with C3H-derived B cells developed in C3H/C3H chimeras. iv) Evidence was obtained suggesting that stimulation of antibody response by allogeneic effect in the absence of syngeneic or semisyngeneic helper T cells did not take place in this experimental system. v) With the use of congenic resistant strains, it was shown that alloantigens controlled by H-2 loci, in particular by the K-I region of this gene complex, constituted the barrier of cooperative interaction between histoincompatible T and B cells. vi) Cooperation between H-2 compatible, non-syngeneic T and B cells was also disturbed in varying degrees depending on the strain combinations, thus indicating that cell surface antigens controlled by non-H-2 loci also had a significant role for the cooperative interaction between T and B cells. Problems associated with these findings were discussed.

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PubMed1976

[Stimulant effect of antilymphocytic serum on early stages of hematopoietic recovery in the spleen of radiation chimeras].

Experiments conducted on 236 BALB/c mice were aimed at the study of the effect of the antilymphocytic serum on the hemopoiesis recovery in the spleen of the radiation chimeras, since the antilymphocytic serum was known to increase the number of macroscopic hemopoietic colonies. This increase was found to be due to the intensification of the first hemopoietic recovery stage, i.e. to the acceleration and intensification of the reticular cell activation in the recepient's spleen.

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PubMed1975

Rat-mouse radiation chimeras: characterization of an antibody-mediated graft-vs-host reaction.

A modification of the Jerne hemolysis-in-agar technique was used to demonstrate antibody-mediated graft-vs-host (GvH) hemolytic activity in lymphoid tissues of rat-mouse radiation chimeras. Initial foci of hemolytic activity were detected on the 3rd day in spleens of lethally x-irradiated mice infused with rat spleen cells (950 R-RSp chimeras). The peak of GvH foci response occurred near the end of the 1st week when 70% of 950 R-RSp chimera spleens examined contained an average of 18 to 21 foci per spleen. GvH hemolytic activity was also detected in mice reconstituted with rat bone marrow (950 R-RBM chimeras); however, only 40% of these chimeras contained splenic foci (nine foci per spleen) on day 8, the peak day of response. Mesenteric lymph nodes from 950 R-RSp chimeras, but not 950 R-RBM chimeras, also contained GvH hemolytic foci. Specificity experiments demonstrated that the GvH hemolytic reaction could be inhibited with rabbit anti-rat IgM serum and host (C3BF) antigenic cell fragments. Indirect (IgG) hemolytic activity was also observed in spleens of 950 R-RSp chimeras 6 to 10 days after treatment. At least 90% of indirect foci appeared coincident with direct foci. Rat IgM and IgG containing cells beneath hemolytic foci were observed by combining the fluorescent antibody and foci techniques. To determine whether the foci response reflects and in vivo sensitization of donor cells, spleen cell transfer experiments were done. The results indicate that spleen cells from 950 R-RSp chimeras were more effective in acelerating mortality and anemia and induced a higher incidence of Coomb's positive red cells in lethally irradiated isogeneic recipients than spleen cells from 950 R-RBM chimeras; spleen cells from either chimera were more effective in accelerating GvH indices than spleen and marrow cells from normal rats.

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PubMed1979

Patterns of virus-immune T-cell responsiveness. Comparison of (H-2k X H-2b) leads to H-2b radiation chimeras and negatively selected H-2b lymphocytes.

Negatively selected H-2K(b)D(b) TDL can be induced to respond strongly to vaccinia virus presented in the context of both H-2K(k) and H-2D(b) when stimulated in irradiated H-2K(k)D(b) recipients. Addition of excess (H- 2K(k)D(b) x H-2K(b)D(b))F1 TDL, which are low responders to H-2D(b)-vaccinia virus, does not obviously suppress the reactivity pattern of the H-2K(b)D(b) T cells. However, lymphocytes from chimeras made by reconstituting H- 2K(b)D(b) mice with (H-2K(k)D(k) x H-2K(b)D(b))F(l) bone marrow cells make little, if any, cytotoxic T-cell response to vaccinia virus when sensitized in H-2K(k)D(b) recipients. We have thus documented one instance where the responder phenotype of T ceils from an F(l) {arrow} parent chimera is not equivalent to that associated with the H-2 type of the parental thymus. Lymphocytes from both the chimera and the H-2K(b)D(b) parent (after negative selection) are tolerant to the H-2K(k) and I-A(k) alloantigens encountered in the recipient, but the chimera T cells are also defective in their response to a neoantigen (vaccinia virus) presented in the context of H-2K(k) which the parental T cells invariably recognize. It is thus possible that at least part of the phenomenology associated with the F(l) {arrow} parent radiation chimeras reflects deletion of repertoire in the context of H-2 antigens present during thymocyte ontogeny on other than radiation-resistant thymic epithelium.

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PubMed1978

Induction of allogeneic unresponsiveness in adult dogs. Role of non-DLA histocompatibility variables in conditioning the outcome of bone marrow, kidney, and skin transplantation in radiation chimeras.

Exposure to supralethal total body irradiation and transplantation of bone marrow from a DLA- and pedigree-identical donor have regularly produced successful engraftment and the establishment of stable long-term chimerism in beagles of the Cooperstown colony. Bone marrow allografts performed in pairs of dogs bearing identical DLA haplotypes derived from different pedigree origins (i.e., different classes of the same haplotype) yielded two different results. Depending upon the particular haplotype pedigree combination used, such transplants either led to long-term chimerism or to failures of engraftment, secondary disease, and death of the recipients (i.e., pedigree-incompatible combinations). Radiation chimeras given bone marrow from a DLA-and pedigree-identical donor were challenged within 8-12 h after marrow transplantation with a renal allograft obtained from another DLA- and pedigree-identical donor. The recipients have remained unresponsive to such renal allografts and have survived indefinitely with normal renal function. In contrast, renal allografts obtained from donors bearing the same DLA haplotypes derived from pedigree-incompatible sources were rejected within 25-50 days after transplantation. The long-term surviving recipients have also been unresponsive to skin allografts obtained from their donor of marrow and the kidney donor. Skin grafts obtained from other DLA- and pedigree-identical dogs were rejected within 13-41 days, and grafts from DLA-incompatible donors survived for 10-25 days. These results highlight the potential importance of genetically controlled histocompatibility determinants other than DLA in conditioning allograft reactivity. The determinants uncovered in the present study appear to be linked to the DLA complex, as demonstrated by the ability of the pedigree origins of DLA haplotypes present in individual dogs to serve as an effective marker system for such non-DLA antigen(s). The results also point to the potential usefulness of the early postirradiation period for the induction of allogeneic unresponsiveness in large adult mammals.

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PubMed1975

Potentiating effect of fetal thymus on fetal liver cells for the promotion of recovery from the radiation injury in murine allogenic radiation chimeras or a little bit of thymus goes a long, long way.

Lethally irradiated CBA (H-2k) mice were treated with small numbers of liver cells from strain-A (H-2a) fetal donors. Recovery from the radiation injury was dependent upon the dose of liver cells administered. Giving very small numbers of fetal thymus cells, in addition to liver cells, had a highly significant and salutary effect on survival. The results suggest that clinical transplantation of liver cells from a single fetus might succeed if thymus cells are added.

Animals↗
PubMed1977

[Immunofluorescent study of the hemopoietic organs of xenogeneic mouse radiation chimeras].

An immunofluorescent study of hemopoietic organs in xenogenic (mouse-rat) radiation chimaeras has been carried out by means of specific antiserum against hemopoietic cells of the rat bone marrow. The presence of donor cells was tested at different times after the transplantation in the bone marrow, spleen, lymph nodes, thymus and liver of radiochimaeras. The transplanted cells were shown to populate all hemopoietic organs of the recipient, first of all tissues of the bone marrow type and, then, lymphoid organs. The donor (bone marrow) origin of the extramedullar foci of hemopoiesis in the liver was established.

Animals↗
PubMed1978

[Immunofluorescent study of the origin of connective tissue cells in xenogenic radiation chimeras under normal conditions and in aseptic inflammation].

The origin of elements of the focus of aseptic inflammation and the normal subcutaneous connective tissue in the xenogenic (mouse-rat) radiation chimaeras was investigated by means of indirect Coons method with antiserum to the rat bone marrow cells. The cells of the imflammation focus (leucocytes, macrophages, fibroblasts or fibroblast-like cells, polynuclear giant cells of foreign bodies), as well as leucocytes, macrophages and some fibroblasts of the normal subcutaneous connective tissue, were shown to take their origin from the transplanted bone marrow cells of the donor.

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PubMed1975

[A radioautographic study of the turnover and differentiation of mast cells in normal mice and mouse radiation chimeras].

The patterns of renewal of the previously labeled by 35S-sulphate mast cells of peritoneal liquor and loose connective tissue were investigated in normal mice, after their irradiation and transplantation of singenic and xenogenic bone marrow (radiation mouse chimaeras). The renewal of labeled mast cells in the peritoneal liquor proceeds markedly (ca. 10 times) more intensively than in the loose connective tissue. A stage of lymphocyte-like cells-precursors actively synthesizing sulphomucopolysaccharides is established in the series of differentiation of mast cells during postnatal ontogenesis. The duration of this stage amounts to 10-15 days. The patterns of renewal of the previously labeled by 35S-sulphate mast cells do not differ markedly in normal animals and radiation chimaeras.

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