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Biomedical subjects

C B Carpenter

Publications and source records attributed to C B Carpenter.

At least 217 records · Page 12Linked to original sources
PubMed1975

Surface properties and functional characteristics of infiltrating cells harvested from acutely rejecting cardiac allografts in inbred rats.

Viable, functioning effector cells exerting donor specific cytotoxic properties have been removed, with their surface properties intact, from acutely rejecting cardiac allografts in rats to define immunological events occurring within the grafts themselves. Macrophages comprised 15 to 25% of the cells harvested; lymphocytes comprised about 75%. A few polymorphonuclear leukocytes (approximately 5%) were present consistently. Lymphocytes bearing surface Ig, B cells, made up 35 to 47% of the mononuclear cells collected. The remaining lymphocytes were presumptive T cells. The surfact attributes of the infiltrating cells were compared to those of cells from recipient peripheral blood, spleen and lymph nodes, and to those from isografted controls. Many of the B lymphocytes possessed Fc receptors but were virtually unable to form erythrocyteantibody complement (EAC) rosettes, in contrast to splenocytes which formed approximately 30% EAC rosettes. Specific cytotoxicity against donor alloantigen-bearing cells, as tested in a 51Cr release assay, was shown to be a T cell function by serial fractionation experiments. Peak cytotoxicity of infiltrating T cells occurred early during the rejection process, while that of cells from recipient blood and lymphoid tissues occurred only following complete graft destruction. Antibody-dependent lymphocyte-mediated cytotoxicity (Ab-LMC) was demonstrated following gentle trypsinization or overnight incubation of the cells. Differing effector cell populations could be distinguished by treatment of anti-Ig and complement; direct donor-specific lymphocyte-mediated cytotoxicity was not disrupted by this treatment, while Ab-LMC was abolished.

Animals↗
PubMed1975

Modification of the rat alloimmune response by enhancing antibodies and the role of blocking factors in the survival of renal grafts.

Correlation of morphological and immunological events ocurring in control and passively enhanced rat renal allograft recipients has revealed an important role for vasculitis in rejection, whereas the tempo and severity of graft lymphocyte infiltration and tubular damage was comparable in both groups during the first 5 days. Thereafter, the degree of cellular infiltration in enhanced allografts progressed and actually exceeded that in control grafts. 2-Mercaptoethanol-sensitive lymphocytotoxic antibodies were present in both groups with comparable titers and appearance times; however, the presence of a severe IgG-containing necrotizing arteritis and glomerulitis in control, but not enhanced, grafts suggests that passive enhancement protects by interfereing with the cooperative T cell-dependent inductive response. Further support for this possibility comes from the fact that the development of cytotoxic lymphocytes against donor target cells was delayed for 48 hr in the enhanced group. While controls died at days 9-11, enhanced animals entered a period of prolonged survival with stable renal function. This state of "autoenhancement" was characterized by a low degree of cell-mediated cytotoxicity and the appearance of serum factors that blocked the in vitro cellular assay. Blocking factors have a low affinity for the attacking cell population, suggesting that they are immune complexes or anti-idiotypic antibodies, and not free alloantibody of high affinity.

Animals↗
PubMed1975

Immunologic enhancement of rat renal allografts. III. Immunopathologic lesions and rejection in long-surviving passively enhanced grafts.

Immunologic enhancement of renal allografts from (Lewis times Brown Norway) F1 to Lewis rats was achieved by administering a single dose of antidonor serum at the time of transplantation. A series of grafts functioning for 1 to 4 months after transplantation were examined by light and immunofluorescence microscopy to evaluate the long-term protective effects of the enhancing serum and to determine if previously unobserved lesions appeared in long survivors. Despite the absence of detectable circulating cytotoxic alloantibody, long-term allografts showed necrotizing glomerular and arterial lesions which resembled those seen in acutely rejecting grafts and were compatible with humoral rejection. Thus, in this model, there is a late decline in the ability of passive enhancement to inhibit humoral rejection. Long-term grafts also developed tubular lesions with deposition of immunoglobulin and complement on the tubular basement membranes (TBM). Anti-TBM antibodies were demonstrated in recipients' sera and found to be organ specific but not major histocompatibility antigen or species specific. This tubular lesion is therefore a unique form of allograft injury in which the immune response is directed against tissue antigen(s) which are distinct from the major histocompatibility antigens that induce rejection.

Animals↗
PubMed1975

The effects of varying dialysis regimens on lymphocyte stimulation.

A protocol was designed to alter mean time average serum concentrations of "middle" (B12) and "small" (urea) molecules. Serum before and after studies was tested for its effect on the blastogenic response to PHA. From this study we have concluded that: 1. Serum of patients on hemodialysis inhibits the mitogenic response of normal lymphocytes to PHA when compared to normal sera. 2. This phenomenon is not responsive to pertubations in dialysis designed to alter the concentration of ""middle'' and ""small'' molecules. 3. The inverse correlation between PHA response and serum PO4 and likewise the inverse correlation with changes in bone X-rays suggest that PTH, fragments thereof, or other factors related to bone and calcium metabolism, could conceivably be involved. This could mediated via cyclic AMP.

Adult↗
PubMed1975

Augmentation of proliferation and in vitro production of cytotoxic cells by 2-ME in the rat.

Low concentrations (10(-5) to 10(-8) M) of 2-mercaptoethanol (2-ME) greatly enhance the proliferation of allogeneic cells in the rat mixed lymphocyte culture (MLC). Studies were undertaken to determine the mode of action of 2-ME. MLC proliferation can occur in the absence of serum proteins (fetal calf serum, FCS) only if 2-ME is present; however, a synergistic effect is present with FCS plus 2-ME, with a 3-fold increase in 3HTdR incorporation with FCS concentrations as low as 0.1%. Kinetic studies show no shift in the peak of proliferation (92 hr) when comparing cultures with and without 2-ME; however, 2-ME-supplemented cultures have significant 3HTdR uptake at 24 hr, and the peak amount of uptake at 92 hr is two to four times higher. Delayed addition of 2-ME until 92 and 166 hr produces a further increase in 3HTdR uptake, indicating that the entire effect is not expressed at the time of allogeneic recognition. L-ascorbic acid, another reducing agent which lacks sulfhydryl groups, elicits a much lower effect on DNA synthesis than does 2-ME. The cytotoxicity of cells harvested from MLC supplemented with 2-ME is increased without loss of target specificity, whereas the same concentration of 2-ME has no direct effect upon the cytotoxicity assay except at higher concentrations where 2-ME suppresses cytotoxicity.

Animals↗
PubMed1974

Cholinergic augmentation of lymphocyte-mediated cytotoxicity. A study of the cholinergic receptor of cytotoxic T lymphocytes.

Cholinergic agonists have previously been shown to augment the ability of sensitized lymphocytes to injure cells bearing the sensitizing alleantigens. The cholinergic receptor of the attacking lymphocyte population has been studied with pharmacological manipulation of an in vitro system that quantitates the injury mediated by sensitized attacking cells upon target cells. The data reveal that muscarinic ligands are several orders of magnitude more potent than nicotinic agents in altering cytotoxicity.

Animals↗
PubMed1974

Immunologic enhancement of rat renal allografts. I. Comparative morphology of acutely rejecting and passively enhanced grafts.

The acute unmodified rejection of (Lewis x Brown Norway) F(1) to Lewis renal allografts is characterized by an early and progressive lymphoid cell infiltrate, glomerular necrosis, necrotizing arteritis and ischemic cortical necrosis leading to graft destruction. A single low dose of enhancing antiserum given at the time of transplantation prolongs graft survival by abrogating the necrotizing lesions in glomeruli and arteries and the subsequent cortical necrosis. Passive enhancement in this model is interpreted as representing predominantly a block in the humoral antibody-mediated rejection response. It is suggested that the block is effected mainly, peripherally, ie, at the level of the transplanted kidney itself.

Animals↗