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Biomedical subjects

J P Merrill

Publications and source records attributed to J P Merrill.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1974

Immunologic enhancement of rat renal allografts. II. Immunohistology of acutely rejecting and passively enhanced grafts.

Unmodified renal transplants from (Lewis x Brown Norway) F(1) hybrids to Lewis rats show deposition of immunoglobulin (IgG) and complement in the arteries, which cause an acute necrotizing arteritis with ischemic necrosis of the grafts. Treatment with a single dose of enhancing antiserum at the time of transplantation prevents the arterial deposition of IgG and complement, and the vascular lesions. The enhancing antibody probably acts peripherally by blocking crucial antigenic sites in the graft vasculature, since cytotoxic alloantibody is detectable in the circulation of both control and enhanced recipients. Unmodified allografts also show deposition of IgG in glomeruli accompanied by glomerular necrosis. Immunofluorescent studies indicate that these glomerular lesions are mediated by complexes of antigen and alloantibody, and at least partially also by a nonhistocompatibility antibody directed against antigens in glomerular endothelial cells. Enhancing antiserum treatment reduces glomerular IgG deposition and thus greatly mitigates the glomerular lesion as well.

Animals↗
PubMed1973

The modulating influence of cyclic nucleotides upon lymphocyte-mediated cytotoxicity.

The capacity of allosensitized thymus-derived lymphocytes to destroy target cells bearing donor alloantigens is modulated by the cellular levels of cyclic AMP and cyclic GMP. Increases in the cyclic AMP levels of attacking lymphocytes by stimulation with prostaglandin E(1), isoproterenol, and cholera toxin inhibit lymphocyte-mediated cytotoxicity; whereas, depletion of cyclic AMP with imidazole enhances cytotoxicity. The augmentation of cytotoxicity produced by cholinergic stimulation with carbamylcholine is not associated with alterations in cyclic AMP levels and is duplicated by 8-bromo-cyclic GMP. The effects of activators of adenylate cyclase, cholinomimetic agents, and 8-bromocyclic GMP are upon the attacking and not the target cells and occur at the time of initial interaction of attacking and target cells. Indeed, the level of cyclic nucleotide (cyclic AMP and cyclic GMP) at the time of initial cell-to-cell interaction determines the extent of cytotoxicity.

Animals↗