Toxoplasmosis: the need for improved diagnostic techniques and accurate risk assessment.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
The C3b receptor of human erythrocytes, neutrophils, monocytes, all mature B cells, a subpopulation of T cells, and glomerular podocytes is a single chain glycoprotein that exists in two allotypic forms having Mr's of approximately 250,000 (F) and 260,000 (S). The number of receptors present on erythrocytes varies by eight-fold among different individuals and is genetically regulated by two codominant alleles that are distinct from the alleles determining the structural polymorphism. The number of receptors expressed by neutrophils is subject to rapid increases from 5000 per cell to 40,000 per cell by exposure to nanomolar concentrations of C5adesArg, in vitro, and a similar mechanism is probably the basis for observing increased receptor expression on neutrophils in patients undergoing hemodialysis. Cytoskeletal association of the C3b receptor on monocytes and neutrophils is suggested by experiments demonstrating receptor-mediated phagocytosis, adsorptive endocytosis through coated pits, and restricted lateral diffusion, and by the reciprocal co-redistribution of cross-linked C3b and Fc receptors, and the detergent-insolubility of cross-linked C3b receptors. The factor H-like cofactor activity of the C3b receptor promotes the cleavage of bound C3b to iC3b, C3c and C3d, g, reactions that may enhance the clearance of circulating immune complexes and the generation of ligands for CR2 and CR3. The inherited partial deficiency of erythrocyte C3b receptors in patients with SLE, and the absence of glomerular C3b receptors in these patients with proliferative glomerulonephritis may contribute to systemic and organ-specific abnormalities in the clearance of immune complexes that contribute to the pathogenesis of this disease.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The effects of fluoride (F) on neutrophil protuberance formation and induced Con A acceptor molecule migration were assessed microscopically. Below 5 mM, F had little effect on acceptor migration, while it markedly inhibited formation of colchicine-induced protuberances. The anion also increased the rate at which preformed protuberances regressed. Since protuberance formation is enhanced by disassembly of microtubules, these data suggest that F promotes and/or stabilizes microtubule assembly. Microtubule assembly is favored by binding of GTP to tubulin subunits, while GDP binding favors disassembly of microtubules. Since F binds with GDP, forming a new complex that mimics GTP, the anion would be expected to enhance microtubule assembly. Over the same F concentration range, the anion failed to inhibit acceptor polarization, but did inhibit cytochalasin B-enhanced dispersion of prepolarized Con A acceptors, implying that, at low concentrations, F also affected microfilament cycling. Concentrations of F in excess of 5 mM inhibited acceptor migration as well as protuberance formation. At 20 mM, the anion abolished both events, yet at this same concentration F induced neutrophil superoxide generation and degranulation, suggesting that acceptor migration is not a prerequisite for these two neutrophil effector activities.
A panel of monoclonal antibodies and ligands that bind to the CR1 or CR2 complement receptors of B cells has been used to investigate the role of these membrane molecules in regulating B-cell proliferation and differentiation. When CR2 was modulated from the surface of B cells by treatment with the HB-5 antibody and a secondary goat anti-mouse immunoglobulin antibody, Epstein-Barr virus-induced polyclonal B-cell proliferation and immunoglobulin production were inhibited by 83 and 90%, respectively. In contrast, modulation of other cell surface molecules, HB-2, B1, and the C3b receptor (CR1), or pretreatment of B cells with C3d,g (a CR2 ligand) or HB-5 antibody, alone minimally inhibited these responses. Neither the HB-5 antibody C3d,g, nor a monoclonal antibody (YZ-1) reactive with CR1 induced resting B cells to proliferate, nor did they alter anti-mu antibody-induced proliferation. Similarly, treatment with C3d,g or with the HB-5 or YZ-1 antibodies did not induce B cells to secrete immunoglobulin or affect pokeweed mitogen-induced plasma-cell formation. Whereas CR2 appears to be the functionally relevant receptor for Epstein-Barr virus on B cells, the effects of ligand interactions with CR1 and CR2 on normal B-cell proliferation or differentiation remain unidentified.
In the present study, a panel of six individual hybridoma derived antibodies produced against the BK strain of Toxoplasma gondii were evaluated for their reactivity in an immunofluorescence test. Each of the six monoclonal antibodies demonstrated a unique pattern of fluorescence localized to distinctive regions on the toxoplasmas. Although all of the six detected antigenic determinants which were shared by at least four different T. gondii strains, monoclonal antibody TG-E4A17 has disclosed hitherto unrecognized population differences among the BK or PH strain parasites. The fact that some of the antigenic molecules are restricted to distinct regions of the toxoplasmas may have implications in the infections process/immune response.
The reaction was studied of the J5-monoclonal antibody with the common acute leukemia antigen (CALLA) on non-malignant human tonsil lymphatic cells, which were double labelled also with antibodies against the B1 and HLA-DR antigens or the kappa and lambda light chains. There were few cells (mean 0-1.4%) which were positive with J5 but not B1. Other percentages of labelled cells depended on the order in which the antibodies were added. If the J5-antibody was added first, more B1 positive cells are found than if the B1 antibody is added first. Similarly, a significant (p less than 0.01-p less than 0.001) increase (3.3-18.8%) in the percentage of cells positive with J5 was found when the B1, kappa, and HLA-DR antibodies were added first, but not if antibody against lambda chains is added first. This difference was most pronounced and most significant for B1. This difference can be explained inter alia by steric differences between antibody conjugated and non-conjugated antigens followed by unmasking of other antigens. Double labelling is thus not equal to two single labellings.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.