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PubMed1979

Adaptive differentiation of murine lymphocytes. II. The thymic microenvironment does not restrict the cooperative partner cell preference of helper T cells differentiating in F1 leads to F1 thymic chimeras.

The cooperating preference of helper T cells originating from F1 bone marrow, but differentiating in adult thymectomized, lethally irradiated F1 recipients reconstituted with either f1 or homozygous parental thymus grafts was investigated. Cooperating preference was assayed by determining the levels of helper activity provided by antigen-primed T cells derived from such thymic chimeras for hapten-primed B lymphocytes obtained from conventional F1 or parental donors in adoptive secondary antibody responses in vivo. The results of these analyses revealed a tendency of helper T cells derived from parental thymic chimeras to provide better help for B cells of the same parental type corresponding to the origin of the thymus graft than for the opposite parent. Such preference was, however, only marginal and rarely were differences in levels of helper activity provided to the respective parental types statistically significant. Moreover, this marginal preference, when observed, pertained only to responses of the IgG class; no concordant preference in providing helper activity for IgE antibody responses was observed even with the same populations of thymic chimera helper T cells. Finally, in no instance was there any evidence of restriction in the classical sense of presence versus absence of help as we have routinely observed in all of our previous studies concerning genetic restrictions of T-B-cell cooperative interactions. Although the basis for differences in the studies reported here when compared to observations made in cytotoxic T-lymphocyte systems is unclear, and could reflect genuine mechanistic requirements concerning what directs H-2 restrictions in helper T cells and cytotoxic T lymphocytes, respectively, it is also possible that we are placing too much faith in our interpretations of data obtained in bone marrow chimera systems than is perhaps justified by the potentially great fragility of such systems.

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PubMed1979

T-helper function of parent leads to F1 chimeras. Presence of a separate T-cell subgroup able to stimulate allogeneic B cells but not syngeneic B cells.

Parent leads to F1 chimeras were prepared by reconstituting sublethally irradiated H-2 heterozygous mice with marrow cells from one parental strain. Purified parental strain T cells prepared from unprimed chimeras were exposed to sheep erythrocytes in heavily irradiated mice of each of the two parental strains and recovered from thoracic duct lymph of the recipients at either day 1 or day 5 posttransfer. The lymphoborne cells were then tested for their capacity to collaborate in vivo with B cells of the two parental strains. From this approach it was concluded that parent leads to F1 chimera T cells contain two discrete subgroups of T-helper cells, one specific for self H-2 determinants and the other restricted to H-2 determinants of the opposite parental strain. The restrictions mapped to the K-end of the H-2 complex.

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PubMed1979

Natural, genetically determined resistance toward influenza virus in hemopoietic mouse chimeras. Role of mononuclear phagocytes.

Radiation chimeras produced by crosswise transfers of bone-marrow cell among histocompatible mice susceptible, or genetically resistant, to lethal challenge by a number of myxoviruses were used to test whether macrophage resistance (as assessed in vitro) and resistance of the animal (as measured in vivo), both previously shown to be brought about by the gene Mx, were causally related. 49 chimeras were tested individually, both of resistance of their macrophages to in vitro challenge with M-TUR (a strain of avian influenza virus A/Turkey/England/63 adapted to grow in cultured mouse peritoneal macrophages), and for resistance of the animal in vivo upon challenge with pneumotropic, neurotropic, or hepatotropic influenza viruses. Cultivated Kupffer cells and peritoneal macrophages harvested from chimeric mice expressed the resistance phenotype of the bone-marrow donor irrespective of the host environment in which they had differentiated. However, susceptibility or resistance in vivo was according to the genotype of the host. Thus, inborn resistance of radiation chimeras was found to be independent of Mx-gene expression in cells of the hemopoietic system.

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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.

Animals↗
PubMed1975

Allogeneic unresponsiveness to orthotopic cardiac transplants in DL-A-identical radiation chimeras.

Nine Cooperstown beagles of known DL-A genotypes were exposed to supralethal total-body irradiation and received bone-marrow allografts from DL-A-identical donors. Four to 5 months later, the resulting chimeras received orthotopic cardiac allografts from their corresponding donors of marrow. Six chimeras died of operative complications in the immediate postoperative period. The other 3 chimeras survived from 173 to 547 days; 1 dog died at 173 days as a result of right-sided heart failure, secondary to stenosis at the site of the pulmonary artery anastomosis. The other two recipients continue to be active and healthy at 545 and 547 days. The results indicate that dogs can be rendered specifically tolerant to orthotopic cardiac allografts by supralethal total-body irradiation and the transplantation of marrow obtained from the prospective allograft donor.

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PubMed1979

Mitochondrial malic enzyme in mosaic skeletal muscle of mouse chimeras.

The question was investigated whether mitochondria in the mammalian skeletal muscle fiber syncytium incorporate gene products encoded by one or many nuclei. Mouse chimeras were produced from strains which differ in their electrophoretic variants of the nuclear-coded mitochondrial protein, malic enzyme (MOD-2, E.C. 1.1.1.40, L-malate NADP+ oxidoreductase decarboxylating). The MOD-2 phenotypes of skeletal muscles of these chimeras were characterized in a starch gel electrophoretic system. The results indicate that individual mitochondria can contain products encoded by multiple nuclei and therefore that, for skeletal muscle mitochondria, the cell is not subdivided into nuclear territories. Possible mechanisms of gene product distribution in skeletal muscle fibers are discussed.

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PubMed1979

Staggerer chimeras: intrinsic nature of Purkinje cell defects and implications for normal cerebellar development.

The site of gene action of the Staggerer mutation of mice was investigated with Staggerer in equilibrium or formed from wild-type chimeras. Homozygous Staggerer mice show severe locomotor difficulties due to cerebellar abnormalities which include degeneration of virtually all granule cells and cytological defects in Purkinje cells. Although the locomotor deficits of the mutant were not present in the chimeras, the presence of Staggerer cells affected cerebellar structure. The size and the extent of foliation of the chimeric cerebella were intermediate between wile-type and homozygous Staggerer. A normally proportioned granule cell layer was present. Using beta-glucuronidase as an independent determinant of a cell's genotype, it was found that the genotypically Staggerer medium-to-large neurons expressed all of the light microscopic defects observable in these cells in the homozygous mutant. These defects include: (1) smaller size; (2) usually ectopic location; and (3) regional variation in the cytological appearance of the perikaryon. By contrast, all Purkinje cells which were genotypically wild-type appeared normal in size, in location and in their cytological appearance. Their density, however, was much reduced from wild-type. The effects of the Staggerer mutation on the granule, stellate and basket cells could not be directly assessed as the glucuronidase marker is not suitable for use with these cells. The Staggerer gene thus acts directly on Purkinje cells rather than via extracellular environmental changes. The findings are discussed in terms of their implications for normal cerebellar development.

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PubMed1975

Histocompatibility studies in a closely bred colony of dogs. V. Mechanisms of cellular adaptation in long-term DL-A identical radiation chimeras.

20 Cooperstown beagles of known DL-A genotypes (B" dogs) were exposed to supralethal total body irradiation and received a bone marrow allograft from a DL-A identical donor (A" dog); the resulting chimeras have survived uneventfully for 882, 1466 days, with no evidence of secondary disease, and have been tolerant to kidney and skin allografts obtained from the donor of marrow. Treatment of "A" dogs with serum obtained from their long-term "B" chimeras had no significant effect upon the ability of the recipients to reject "B" skin allografts...

Animals↗
PubMed1976

H-2 restriction of virus-specific cytotoxicity across the H-2 barrier. Separate effector T-cell specificities are associated with self-H-2 and with the tolerated allogeneic H-2 in chimeras.

During infection with lymphocytic choriomeningitis or vaccinia virus, F1 irradiation chimeras reconstituted with bone marrow cells from or both parents generate cytotoxic T cells which can lyse targets across the H-2 barrier. However, activity of chimera T cells is H-2 restricted as shown by cold target competition experiments and selective restimulation of a secondary response in vitro; T cells of H-2k specificity which lyse tolerated infected H-2d target cells do not lyse infected H-2k or unrelated target cells and vice versa. Therefore, H-2 restriction of virus-specific cytotoxic T cells probably does not reflect need for like-like self-interactions for lysis to occur. The specificity of virus immune T cells is thus determined by the H-2K and H-2D specificities present in the infected animal and which are probably recognized unidirectionally by T cells. The results are compatible with the idea the T cells are specific for "altered alloantigen", i.e., a complex of cell surface marker and viral antigen. Alternatively, explained with a dual recognition model, T cells may possess two independently, clonally expressed receptors, a self-recognizer which is expressed for one of the syngeneic or tolerated allogeneic K or D "self" markers, and an immunologically specific receptor for viral antigen.

Animals↗
PubMed1978

Restricted helper function of F1 leads to parent bone marrow chimeras controlled by K-end of H-2 complex.

F1 leads to parent bone marrow chimeras were prepared by transferring F1 hybrid marrow cells into heavily irradiated parental strain mice. When unprimed, donor-derived F1 T cells from the chimeras were activated to sheep erythrocytes (SRC) for 5 days in irradiated normal F1 mice, high IgM and IgG anti-SRC responses were observed with F1 B cells, and with B cells H-2-compatible with the strain in which the T cells were raised from stem cells. Significantly, however, responses with B cells of the opposite parental strain were either absent or very low. The restriction in T-helper function mapped to the K-end of the H-2 complex and could not be attributed to active suppression.

Animals↗
PubMed1978

In a fully H-2 incompatible chimera, T cells of donor origin can respond to minor histocompatibility antigens in association with either donor or host H-2 type.

Fully H-2 incompatible radiation chimeras were prepared using BALB congenic mice. Such chimeric mice were immunized in vivo against histocompatibility antigens of the C57BL/10Sn (B10) background in association with either of the parental H-2 haplotypes, and their spleen cells subsequently boosted in vitro with the same minor antigens. Strong H-2-restricted cytotoxic activity against minor antigens was detected, and the specificity of the restriction could be to the H-2 haplotype of the donor or the host depending on the cells used for priming or boosting. Cross priming could also be demonstrated in these mice. The results show that fully allogenic radiation chimeras can produce H-2-restricted T-cell responses to minor histocompatibility (H) antigens, and are discussed in relation to contrasting results recently obtained against viral antigens.

Animals↗
PubMed1978

Adaptive differentiation of murine lymphocytes. I. Both T and B lymphocytes differentiating in F1 transplanted to parental chimeras manifest preferential cooperative activity for partner lymphocytes derived from the same parental type corresponding to the chimeric host.

The concept of adaptive (selective) differentiation preducts that early differentiation of lymphocytes is conditioned by the environment in which such differentiation takes place. These processes appear to involve selection of lymphocytes according to their self-recognition between interacting lymphocytes is, at least in part, controlled by major histocompatibility complex-linked genes, then adaptive differentiation is also controlled by these genes. In these studies, we have tested the capacities of helper T lymphocytes and hapten-specific B lymphocytes primed in the environments of various combinations of bone marrow chimeras prepared between two parental strains (i.e. A/J and BALB/c) and their corresponding F1 hybrid (CAF1) to interact with primed B and T lymphocytes derived from conventional parent and F1 donors as well as all of the corresponding bone marrow chimera combinations. The results demonstrate clearly that (a) F1 transplanted to F1 chimeric lymphocytes display no restriction in terms of cooperative activity with all of the various partner cell combinations; (b) parent transplanted to F1 chimeric lymphocytes manifest effective cooperative activity only for partner cells from F) or parental donors corresponding to the haplotype of the original bone marrow donor, thereby behaving phenotypically just like conventional parental lymphocytes; and (c) F1 transplanted to parent chimeric lymphocytes display restricted haplotype preference in cooperating best with partner lymphocytes sharing the H-2 haplotype, either entirely or codomimantly, of the parental chimeric host. The implications of these findings for understanding certain controlling mechanisms for lymphocyte differentiation are discussed.

Animals↗
PubMed1978

In irradiation chimeras, K or D regions of the chimeric host, not of the donor lymphocytes, determine immune responsiveness of antiviral cytotoxic T cells.

The H-2 haplotype of the chimeric host determines the responder phenotype of maturing T cells. Spleen cells of chimeric mice formed when (K(k) nonresponder to D(b) x K(b) responder to D(b) plus vaccinia)F(1) bone marrow cells were used to reconstitute K(b)D(b) (C57BL/6 D(b) responder) irradiated recipients generated high levels of D(b) plus vaccinia virus-specific cytotoxic T cells. The same stem cells used to reconstitute K(k)D(b) (B10.A (2R) D(b) nonresponder) irradiated recipients resulted in spleen cells that responded well to K plus vaccinia, but responsiveness to D(b) was low. A generally low response to D(k) plus vaccinia, which seems to be regulated by D(k), was confirmed in chimeras. Thus, K(d)D(d) (D(d) plus vaccinia responder) stem cells differentiating in a K(d)D(k) chimeric host failed to generate a measurable response to D(k) plus vaccinia. In contrast, stem cells from K(d)D(k) (D(k) plus vaccinia low responders) differentiating in a K(d)D(d) (K(d) and D(d) high responders to vaccinia) host do generate responsiveness to D(d) plus vaccinia. These results indicate that in chimeras, the Ir phenotype is independent of the donor T cell's Ir genotype, and that thymic selection of a T cell's restriction specificity for a particular H-2 allele of the chimeric host also defines that T cell's/r phenotype.

Animals↗
PubMed1979

Mosaic analysis of dystrophic embryos aggregated with normal chimeras: an approach to mapping the site of gene expression.

Genotypically dystrophic muscle in mouse chimeras of dystrophic leads to and comes from normal genotype has been influenced to develop normally and remain healthy. A significant extramuscular component that effects the expression of the muscle disease in homozygous dystrophic mice is thereby implicated. The potential application of the chimera preparation in further elucidating the source and the nature of that extramuscular influence is outlined.

Animals↗
PubMed1978

Developmental roles of epithelial and interstitial cell lineages in hydra: analysis of chimeras.

Chimeric hydra were prepared by recombining epithelial and interstitial cells between 3 strains of hydra of different sizes (maxi, normal, and mini strains). The resulting chimeras generally resembled the epithelial cell parent more than the interstitial cell parent in size, budding rate, tentacle number, and form. This suggests that epithelial cells normally exert considerable influence over hydra morphogenesis. However, the chimeras show some differences ascribable to interstitial cell origin. Furthermore, the 3 original strains, when deprived of interstitial cells, lose their distinguishing size differences. Thus both epithelial and interstitial cells (or interstitial cell derivatives) mutually participate in hydra's development.

Animals↗
PubMed1979

Genetic analysis of developmental mechanisms in hydra. VI. Cellular composition of chimera hydra.

The homeostatic mechanisms that maintain constant cellular ratios in hydra tissue were studied using mutant and chimeric hydra strains. Mutants having abnormal cellular compositions are isolated through sexual inbreeding of wild hydra, as described in previous papers of this series. Chimeric hydra are produced by making use of a strain (nf-I) which lacks interstitial cells, nerve cells and nematocytes in its tissue. Reintroduction of interstitial cells from other strains (both normal and mutant) into nf-I leads to creation of chimeric strains having epithelial cell lineages from one strain (nf-I) and interstitial cell lineages from others. Analyses and comparisons of the cellular compositions of all these strains revealed that the numbers of nerve or interstitial cells in the chimeras were very similar to (statistically significantly correlated with) those in their interstitial cell donors. Since chimeras and their interstitial cell donors share the same interstitial cell lineages, this suggests that interstitial cells or their derivatives (nerves and nematocytes) play major roles in determining the nerve and interstitial cell levels in the hydra tissue. It is suggested that some form of homeostatic feedback mechanisms are probably involved in regulating the levels of these cell types.

Animals↗
PubMed1977

[Effect of abrogating hybrid resistance on the survival of radiation chimeras].

A study was made of the effect of the hybrid resistance abrogation by means of the lymphoid cell administration on the survival of the lethally irradiated mice protected by the transplantation of the semiallogeneic bone marrow. Injection to the C57BLxCBA recipients of the C57BL lymphoid cells one day before the irradiation and the transplantation of the bone marrow of the same genotype (C57BL) increased the chimera survival in comparison with the untreated recipients; such pretreatment 7 days before the irradiation decreased the chimera survival. Parental spleen lymphocytes administration produced but an insignificant effect on the radioresistance both of the stem hemopoietic cells (by the endocolonisation test) and of the organism as a whole (by the 30-day survival test) of the F1 hybrid. On this basis a conclusion was drawn that the differences in the splenocyte efficacy, when they were injected at different periods before the irradiation, could not be attributed to the changes in radioresistance.

Animals↗
PubMed1976

C4 synthesis in C4-deficient guinea pig radiation chimeras: restoration of the classic complement pathway.

Bone marrow transplants from normal Albany strain guinea pigs established a functional classical pathway of complement (C) in C4-deficient (C4D) guinea pigs. Seventeen days after transplant the Albany leads to C4D chimeras had detectable C4 and total hemolytic C activities. Maximum C4 levels (2 to 8% of normal were reachered by day 73 and restored total C to 40% of normal. Classical pathway function persisted for about 150 days and, thereafter, declined to undetectable levels by day 385. In contrast, Albany guinea pigs transplanted with C4D marrow maintained normal C4 levels throughout the experiment, suggesting that the C4-producing cells are radioresistant and long-lived. Unlike unmanipulated C4D animals, Albany leads to C4D chimeras were unable to produce antibodies to guinea pig C4 when immunized with normal guinea pig serum. These experiments suggest that bone marrow cell progeny produce C4 in vivo.

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