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T G Wegmann

Publications and source records attributed to T G Wegmann.

100 records · Page 6Linked to original sources
PubMed1971

Immunological tolerance: "forbidden clones" allowed in tetraparental mice.

Tetraparental (allophenic) mice, made chimeric at the eight-cell stage by joining two embryos from histoincompatible parental strains, were examined by a microcytotoxicity test. The results indicate that parental-strain fibroblasts are more effectively destroyed in vitro by lymph node cells from the tetraparental mice than by lymph node cells from the F(1) hybrid or either parental stain. The destruction by tetraparental lymph node cells is indistinguishable from that mediated by lymph node cells from previously immunized allogeneic animals. It can be prevented by serum from the tetraparental mice, but not by sera from the F(1) hybrid or the parental strain animals. The results suggest that a concomitant immunity and serum blocking effect, rather than a central failure of the immune response, may mediate some aspects of normal tolerance.

Animals↗
PubMedDate not supplied

Immune signalling at the maternal-fetal interface and trophoblast differentiation.

In this review the afferent and efferent signals involved in immune signalling at the maternal-fetal interface are highlighted in the light of recent information. MHC antigen expression is reviewed. Immunizing mothers against class I and II MHC antigens can prevent spontaneous fetal resorption in mice. In addition, the CSF family of cytokines is not only secreted in placental tissues, but also play a role in trophoblast proliferation and differentiation. GM-CSF in particular appears to promote trophoblast syncytialization and the synthesis of human chorionic gonadotropin and human placental lactogen. Recent knock-out experiments indicate that CSF-1 is essential for complete fertility. Finally, the fact that the CSF cytokines promote HIV release from macrophages indicates that the knowledge gained in this area could lead to a better understanding of the transmission of the HIV virus from the mother to the fetus through the trophoblast.

Abortion, Spontaneous↗
PubMedDate not supplied

The processing of T-lymphocytes by the but of the suckling neonate.

The suggestion that intact effector lymphocytes can pass from maternal milk through the gut wall of the suckling neonate has been tested directly by labelling alloantigen-stimulated T cells in vitro with [125I]iododeoxyuridine and following their fate after intraoral administration to newborn mice by whole body gamma counting. The cells were rapidly lost from the animal when compared to cells injected intraperitoneally, and at a rate indistinguishable from cells deliberately killed and given intraorally. If the alloantigen used to stimulate the T cells in vitro was shared by the neonate, the T cells were lost even faster. It was also found that highly lethal labelled leukemia cells behaved in a similar fashion and did not cause excess mortality if given intraorally. These results suggest that few, if any, lymphocytes traverse the neonatal gut wall and indicate that subcellular fractions may be responsible for maternal to neonatal transfer of immunological effector functions.

Absorption↗
PubMedDate not supplied

Immunoregulatory effects of lymphokine-driven placental cells on cloned T cells in vitro.

Successful pregnancy is associated with maternal immune sensitization to placental antigens. Placental trophoblast cells at the maternal-fetal interface express histocompatibility antigens of both the maternal and paternal haplotypes. In particular, these paternal-type antigens have the potential to stimulate alloreactive maternal immune responses and, as a result, maternal T cells appear in the decidua shortly after class I major histocompatibility complex encoded antigens are expressed. Despite this maternal immune recognition, immunologic destruction of the fetus rarely occurs. In fact, recent evidence suggests that the interaction between maternal T cells and placental cells results in an "immunotrophic" effect that stimulates placental growth and fetal survival. To better understand the contribution of fetally derived placental cells in the activation of maternal immunity, we have developed a murine lymphokine-dependent long-term placental cell line termed "FRD." FRD cells can stimulate syngeneic, semi-syngeneic, and allogeneic murine spleen cells to proliferate in a mixed lymphocyte-placental cell reaction. Coculture experiments with T hybridomas show that unlike conventional antigen-presenting cells, FRD can activate T cells to secrete lymphokines in the absence of specific antigen. In addition, lymphokine-activated FRD cells release factors that directly stimulate proliferation of the IL 1 responsive T cell line D10.G4.1. These observations suggest that placental cells stimulate T cells via novel mechanisms that may play a role in producing a maternal T cell response that in turn is beneficial to fetally derived tissues during pregnancy.

Animals↗
PubMedDate not supplied

Maternal T cells regulate placental size and fetal survival.

The placental immunotrophism hypothesis states that maternal T cells, through their lymphokines, exert a positive influence on placental growth, which can lead to improved chances of fetal survival. We report here that deleting maternal T cells by monoclonal antibody injection during midgestation is accompanied by increased fetal resorption and decreased placental weight and phagocytosis in two different strain combinations of mice. Conversely, mice with T-cell proliferative disease show increased placental weight and phagocytosis, which can be reversed following T-cell depletion during pregnancy. Furthermore, female mice that are prone to fetal resorption show improved fetal survival if injected with spleen cells from mice with T-cell proliferative disease. These results are in accord with predictions of the placental immunotrophism hypothesis and imply that maternal T cells can participate in the prevention of spontaneous fetal resorption.

Animals↗