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T B Strom

Publications and source records attributed to T B Strom.

At least 325 records · Page 18Linked to original sources
PubMed1978

Specificity of cellular migration into cardiac allografts in rats.

The question has not been previously investigated as to whether host lymphocytes infiltrate vascularized organ allografts in indiscriminate fashion, or whether they are retained selectively because of specific antigenic recognition sites on their surfaces. By using a dual cardiac allograft model in LEW rats, we have examined this problem by two methods: (1) detection of preferentially accumulating cells selectively cytotoxic to allografts bearing specific transplantation antigens as compared with "third-party" allografts; and (2) examination of trafficking patterns of separate radiolabeled populations of sensitized cells adoptively transferred into double heart-grafted recipients. In the first series of experiments, using BN and BUF rats as donors, differences in specific cytotoxicity mounted by infiltrating lymphocytes harvested from the appropriate and inappropriate graft were moderately significant (P less than 0.05). Because the question of cross-reactivity betweeen BUF and BN antigen was raised, lymphocytes sensitized to BN and WF donors were differentially labeled in vitro with 3H- or 14C-thymidine. After mixture and adoptive transfer, the ratio of specific to third-party labels was measured in each graft. In this second series of experiments, significant (P less than 0.001) preferential accumulation of specifically sensitized cells were found in the appropriate vascularized organ allograft. These experiments confirm the results of other experimental models, and demonstrate that sensitized lymphocytes accumulate selectively in specific vascularized organ allografts.

Animals↗
PubMed1978

A characterization of the nature and control of cellular allograft rejection.

The mechanism of cellular rejection has been analyzed. The cells infiltrating rat cardiac allografts have been recovered and identified. An important role for cytotoxic T lymphocytes in cellular rejection has been discerned. The entrapment of cytotoxic T lymphocytes within rejecting grafts is not rigorously dependent upon antigen recognition. The cellular processes by which cytotoxic T lymphocytes destroy target cells have been determined in part. Cellular levels of the 3',5' cyclic nucleotides modulate this process. Elevations in cellular levels of cyclic AMP inhibit cytotoxicity whereas increased cyclic GMP stimulates augmented cytotoxicity.

Animals↗
PubMed1978

A longitudinal study of bone disease after successful renal transplantation.

A retrospective study of 100 patients followed for 1-4 years after successful renal transplantation was undertaken to assess the amelioration of previously present metabolic bone disease and to determine the risk factors associated with the development of osteonecrosis. 42% of patients showed some evidence of bony abnormality. Following transplantation, there was slow but progressive resolution in the X-ray changes of hyperparathyroidism but not of osteoporosis. 14% of patients developed osteonecrosis in the posttransplant period with the femoral head the most common site involved (72% of patients). Osteonecrosis could not be related to average steroid dose, number of steroid pulses, or the preexistence of metabolic bone disease.

Adult↗
PubMed1977

Emergence of insulin receptors upon alloimmune T cells in the rat.

Insulin, as well as other ligands which increase intracellular guanosine 3',5'-cyclic monophosphate (cGMP), augments thymic-derived (T)- lymphocyte effector activity as revealed by alloimmune lymphocyte-mediated cytotoxicity. The observation that insulin binds only to monocytes among circulating nonimmune human mononuclear cells fosterd reexamination of the mechanism by which insulin augments T-lymphocyte function. This report concerns a test of the hypothesis that the T cell is directly affected by insulin and that an insulin receptor emerges upon T lymphocytes consequent to immune activation. Spleens were removed from rats skin grafted across a major histocompatibility barrier. Lymphocytes were harvested from Ficoll-Hypaque density gradients and subsequently enriched for T cells by passage over one or two nylon wool columns. This population was composed of more than 98% T cells as assessed by surface marker techniques (Ig staining, erythrocyte antibody, and erythrocyte antibody complement rosetting, anti-T staining). There was no loss of augmentation of lymphocyte-mediated cytotoxicity induced by insulin, carbamycholine, and 8-bromo-cGMP in the purified cells when compared to unfractionated cells 7 days after transplantation. 125I-insulin bound saturably to the allostimulated T-enriched lymphocytes with maximum binding at 12.8 +/- 0.2 pg and a dissociation constant at equilibrium of 1.3 nM. In contrast, insulin receptors were not present on nonimmune T-enriched cells or on T cells from animals that received syngeneic grafts. The affinity of the lymphocyte insulin receptor was similar to that of more conventional insulin-sensitive tissues e.g., liver, adipocyte. After 89% of T cells from spleens on day 7 were lysed with anti-thy 1.1 antibody and complement, the ability to measure specific insulin binding was lost. These data confirm a physiologic role for insulin in T-lymphocyte effector function and describe the emergence of insulin receptors concomitant with cell sensitivity to ligand. Such receptors may play a role in hormonal modulation of the immune response.

Animals↗
PubMed1977

On the identity of lymphoid cells that stimulate the rat MLC and produce active enhancement.

The preimmunization of 10(7) Brown Norway (BN) rat lymphoid cells i.v. 1 week before (Lew X BN) F1 to Lewis renal grafting causes a state of immunologic enhancement. The BN lymphoid cells responsible for producing enhancement are the same cells that are capable of stimulating Lewis T cells in one-way MLCs. Thus active enhancement requires immunity to LD antigens, since SD +, LD- BN cells do not create a vigorous enhanced state.

Animals↗
PubMed1977

Rapid murine mixed lymphocyte cultures assessed by emergence of T cell insulin receptors.

Murine T lymphocytes incubated in the mixed lymphocyte culture with allogeneic lymphocytes incompatible for the H-2 region or subregions thereof rapidly develop insulin receptors. In contrast, T cells cultured with syngeneic or H-2 and M-locus compatible cells do not develop insulin binding sites. The emergence of insulin receptors may allow rapid HLA-D typing in man.

Animals↗
PubMed1977

Cellular components of allograft rejection: identity, specificity, and cytotoxic function of cells infiltrating acutely rejecting allografts.

Functioning mononuclear cells have been harvested from heterotopic rat cardiac allografts during maximal transplant cellular infiltration. T cells, identified by a T cell-specific absorbed rabbit anti-rat brain serum, constituted two-thirds of the total cells recovered. Approximately 20% of the infiltrating cells bear and synthesize surface immunoglobulin. Macrophages, identified by latex ingestion and morphologic and cytochemical techniques, comprise 9% of the graft infiltrate. Donor-specific cytotoxic T lymphocytes are concentrated within the graft. A separate population of Fc receptor-positive recovered cells mediate antibody-dependent LMC (Ab-LMC). Neither effector cell was adherent or phagocytic. These studies have conclusively established that cytotoxic T lymphocytes accumulate within rejecting allografts; however, the enriched presence of cytotoxic T cells within the grafts is not fully dependent upon antigen recognition per se, since Lew animals grafted with both BN and BUF hearts have Lew anti-BN and Lew anti-BUF killer cells in each graft.

Animals↗