PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Receptors, Immunologic”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1976

Immunological aspects of sperm receptors on the zona pellucida of mammalian eggs.

Sperm receptor sites on the surface of the zona pellucida are believed to be necessary for fertilization on the mammalian egg. Ovary specific antibodies are known to precipitate the zona pellucida and are also responsible for inhibition of sperm binding and subsequent fertilization. The nature of the proposed receptor sites which are blocked by antibodies are discussed relative to comparable studies in which phytoagglutinins and other agents are used to determine the chemical nature of sperm receptor sites.

Animals↗
PubMed1976

Immunological studies of acetylcholine receptors.

Immunochemical techniques for the study of acetylcholine receptors are described. Immunization of rabbits, rats, guinea pigs, and goats with acetylcholine receptor protein purified from Electrophorus electric organ tissue results in muscular weakness and death due to impaired neuromuscular transmission. Serum from immunized animals contains high concentrations of antibodies directed at receptors from the electric organ and low concentrations of antibodies directed at receptors from skeletal muscle. The detailed similarities between the disease of receptor-immunized animals "experimental autoimmune myasthenia gravis" (EAMG), and myasthenia gravis are compared. Reactions of antisera from animals with EAMG with receptor from Electrophorus and Torpedo are studied. Antireceptor antibodies in these antisera are directed predominantly and determinants other than the acetylcholine-binding site.

Acetylcholine↗
PubMed1977

Immunological distinction between acetylcholine receptor and the alpha-bungarotoxin-binding component on sympathetic neurons.

Clone PC12 of a rat sympathetic neuron cell line binds alpha-bungarotoxin and exhibits carbamoylcholine-stimulated uptake of sodium ions. Concentrations of alpha-bungarotoxin that saturate the alpha-bungarotoxin-binding site have no effect on agonist-stimulated sodium uptake. Conversely, antibodies against eel acetylcholine receptor block the agonist-induced sodium flux but fail to recognize the alpha-bungarotoxin-binding component. Detergent extracts of the PC12 clone inhibit the ability of antibody to eel acetylcholine receptor to recognize 125I-alpha-bungarotoxin-acetylcholine receptor complexes derived from muscle. These results distinguish between a ganglionic nicotinic acetylcholine receptor and an alpha-bungarotoxin-binding component on these cells, and provide evidence for antigenic similarities between muscle acetylcholine receptor and ganglionic acetylcholine receptor.

Acetylcholine↗
PubMed1976

Immunology of the thyrotropin receptor.

Antibodies to the thyrotropin receptor appear to be responsible for hyperthyroidism in Graves' disease. The antibodies, described as thyroid-stimulating antibodies (TSAb) mimic the effects of thyrotropin (TSH) by binding to the TSH receptor and activating adenylate cyclase. TSAb consist of an electrophoretically heterogeneous population of IgG and the thyroid-stimulating site is formed by combination of heavy and light chains in the Fab part of the molecule. Binding studies indicate that the TSAb molecule interacts monovalently with membrane bound TSH receptors and that TSAb consists of an antibody population which shows a restricted heterogeneity with regard to TSH receptor affinity. Studies in patients with Graves' disease and hyperthyroidism indicate that the levels of TSAb correlate well with thyroidal iodine uptake and the absence of pituitary control of thyroid function. However in some patients with ophthalmic Graves' disease or autoimmune thyroiditis there is evidence of serum antibodies which interact with the TSH receptor but are unable to stimulate thyroid function.

Antibodies↗
PubMed1976

The immunology of the insulin receptor.

We have detected and characterized anti-insulin-receptor autoantibodies which circulate in several patients with insulin resistance diabetes. These antibodies are predominantly IgG and are polyclonal. They inhibit insulin binding to its receptor on a variety of tissues from widely separated species. Antibodies obtained from different patients appear to bind to different determinants on the receptor and alter receptor function in several ways. Some anti-receptor antibodies are capable of stimulating insulin-like effects on target tissues, while others block insulin-stimulated effects. Direct labeling of anti-receptor antibody with 125I permits use of these antibodies as an assay and probe of insulin receptors.

Adipose Tissue↗
PubMed1976

Immunology of the acetylcholine receptor.

Myasthenia gravis is a spontaneously occurring autoimmune disease in which antibodies and lymphocytes are specifically reactive with nicotinic ACh receptors of skeletal muscle. Antibodies reactive with junctional receptors of human muscle are found in 90% of patients with myasthenia gravis and not at all in other diseases. Their capacity to cross the placenta suggests their involvement in the pathogenesis of neonatal myasthenia. The role of the thymus in myasthenia gravis remains a mystery, but it has a recently been established that the thymus contains nicotinic ACh receptors and that anti-receptor antibodies are present in myasthenic thymuses. Antibodies of myasthenic patients detect only partial cross reactivity between ACh receptors of different species. However, greater antibody binding is observed with receptors isolated from denervated rat muscle than with receptors from normal rat muscle. This suggests that extrajunctional and junctional ACh receptors might express different antigenic determinants. Although human antibodies bind minimally to ACh receptors of the electric organs of eels and marine rays, lymphocyte reactivity to electric eel receptors is found in high incidence in myasthenic patients. This suggests that electric organ and mammalian muscle ACh receptors may share more lymphocyte-defined than serologically-defined antigenic determinants. Both cellular and humoral immune responses to ACh receptors can be induced experimentally. Sufficient antigenic homology exists between receptors of different species that electric organ receptors are capable of inducing in mammals experimental autoimmune myasthenia gravis. Syngeneic muscle receptor also is immunogenic in rats. Induction of both myasthenia and antibodies to ACh receptor requires participation of thymus-derived lymphocytes. The majority of ACh receptors in myasthenic rat muscle exist complexed with antibody, but antibody is not bound directly to the receptor's ACh-binding site. Anti-receptor antibodies in vitro are capable of impairing the electrophysiological function of ACh receptors with minimal blocking of the ACh-binding site and in the absence of complement. Thus, myasthenia gravis and its experimental model provide unique biological tools for studying the structure, function and pathology of cell membrane receptors.

Acetylcholine↗
PubMed2025

Genome-Wide Aggregated Trans Effects Analysis Identifies Genes Encoding Immune Checkpoints as Core Genes for Rheumatoid Arthritis.

OBJECTIVE: The sparse effector "omnigenic" hypothesis postulates that the polygenic effects of common single nucleotide polymorphisms (SNPs) on a typical complex trait are mediated by trans effects that coalesce on expression of a relatively sparse set of core genes. The objective of this study was to identify core genes for rheumatoid arthritis by testing for association of rheumatoid arthritis with genome-wide aggregated trans effects (GATE) scores for expression of each gene as transcript in whole blood or as circulating protein levels. METHODS: GATE scores were calculated for 5,400 cases and 453,705 non-cases of primary rheumatoid arthritis in UK Biobank participants of European ancestry. RESULTS: Testing for association with GATE scores identified 16 putative core genes for rheumatoid arthritis outside the HLA region, of which six-TP53BP1, PDCD1, TNFRSF14, LAIR1, LILRA4, and IDO1-were supported by Mendelian randomization analysis based on the marginal likelihood of the causal effect parameter. Five of these 16 genes were validated by a reported association of rheumatoid arthritis with SNPs within 200 kb of the transcription site, eight by association of the measured protein level with rheumatoid arthritis in UK Biobank, 10 by experimental perturbation in mouse models of inflammatory arthritis, and two-CTLA4 and PDCD1-by evidence that drugs targeting the gene cause or ameliorate inflammatory arthritis in humans. Fourteen of these 16 genes are in pathways affecting immunity or inflammation, and six-CD5, CTLA4, TIGIT, LAIR1, TNFRSF14, and PDCD1-encode receptors that have been characterized as immune checkpoints exploited by cancer cells to escape the immune response. CONCLUSION: These results highlight the key role of immune checkpoints in rheumatoid arthritis and identify possible therapeutic targets.

Humans↗
PubMed2020

Glucocorticoids mobilize macrophages by transcriptionally up-regulating the exopeptidase DPP4.

Glucocorticoids are potent endogenous anti-inflammatory molecules, and their cognate receptor, glucocorticoid receptor (GR), is expressed in nearly all immune cells. Macrophages are heterogeneous immune cells having a central role in both tissue homeostasis and inflammation and also play a role in the pathogenesis of some inflammatory diseases. Paradoxically, glucocorticoids have only a limited efficacy in controlling the resolution of these macrophage-related diseases. Here, we report that the transcriptomes of monocyte-like THP-1 cells and macrophage-like THP-1 cells (THP1-MΦ) have largely conserved gene expression patterns. In contrast, the differentiation to THP1-MΦ significantly altered the sensitivity of gene transcription to glucocorticoids. Among glucocorticoid-regulated genes, we identified the exopeptidase dipeptidyl peptidase-4 (DPP4) as a critical glucocorticoid-responsive gene in THP1-MΦ. We found that GR directly induces DPP4 gene expression by binding to two glucocorticoid-responsive elements (GREs) within the DPP4 promoter. Additionally, we show that glucocorticoid-induced DPP4 expression is blocked by the GR antagonist RU-486 and by GR siRNA transfection and that DPP4 enzyme activity is reduced by DPP4 inhibitors. Of note, glucocorticoids highly stimulated macrophage mobility; unexpectedly, DPP4 mediated the glucocorticoid-induced macrophage migration, and siRNA-mediated knockdowns of GR and DPP4 blocked dexamethasone-induced THP1-MΦ migration. Moreover, glucocorticoid-induced DPP4 activation was also observed in proinflammatory M1-polarized murine macrophages, as well as peritoneal macrophages, and was associated with increased macrophage migration. Our results indicate that glucocorticoids directly up-regulate DPP4 expression and thereby induce migration in macrophages, potentially explaining why glucocorticoid therapy is less effective in controlling macrophage-dominated inflammatory disorders.

Animals↗
PubMed1976

Membrane receptors on neutrophils.

Neutrophils recognise humoral immunologic reactants through 'receptors' on their surface membrane. Most widely studied and probably of greatest biologic significance are the immunoglobulin (Fc), and complement (primarily C3b and C5a) receptors which enable the cell to ract with, and be stimulated by, antigen-antibody, or antigen-antibody-complement complexes and their products. This interaction with the putative receptors and the consequent cell activation occurs most optimally on surfaces and plays a critical role in the mammalian host defense system.

Antibody Specificity↗
PubMedDate not supplied

[Current tests for the "in vitro" immunologic exploration in man].

Several "in vitro" methods are developed to study cellular immunity as same as study of antibodies in humoral immunity exploration. The more used in human pathologics are the enumeration of thymus-derived (T) lymphocytes by the formation of nonimmune rosettes E with sheep erythocytes and bone marrow (B) lymphocytes by the presence of membrane-bound immunglobulins; the detection of lymphocyte activation by measuring proliferation (lymphocyte transformation); the mixed lymphocyte reaction, the elaboration of biologically active mediators (lymphokines) and the lymphocyte-mediated cytoxicity.

Antibodies↗