Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Receptors, Complement”

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.

At least 1,009 records · Page 56Linked to original sources
PubMed1984

Surface immunoglobulin phenotype of complement receptor-positive and complement receptor-negative B cells of normal and xid immunodeficient mice.

Single- and dual-parameter fluorescence-activated cell sorter analyses of complement receptor-positive and -negative (CR+ and CR-) splenic B cells of normal and xid immunodeficient mice were performed to determine the frequencies of surface (s) IgM+ and sIgD+ cells, as well as the quantities of sIgM and sIgD on these cells. Single parameter analysis revealed identical frequencies of sIgM+ and sIgD+ cells in the CR+ B cell population of normal mice. In contrast, the percentage of sIgM+ cells exceeded that of sIgD+ cells in the CR- normal and CR+ xid B cell population to a similar extent. CR- xid B cells showed an even greater discrepancy between sIgM+ and sIgD+ cells. Dual-parameter analysis of CR+ normal B cells showed the typical sIg phenotype of mature B cells, i.e. an intermediate density of sIgM and a high density of sIgD. The CR+ xid B cell population displayed an increase in cells with high sIgM and no-to-low sIgD and a decrease in cells with intermediate sIgM and high sIgD when compared to CR+ normal cells. CR- B cells from normal and xid immunodeficient mice were similar in that both consisted largely of a cell population with low sIgM and no-to-low sIgD. However, the CR- normal B cell population also contained cells with intermediate sIgM and high sIgD, which were lacking in the CR- xid cell population. Similar results were obtained when CR+ and CR- B cells from normal and xid mice were purified from a small resting B cell population, isolated by elutriation. This indicates that the sIg phenotype of CR- cells is not due to the presence of large cells which have lost sIgD during activation.

Animals↗
PubMed1984

Changes in the expression of B cell surface markers on complement receptor-positive and complement receptor-negative B cells induced by phorbol myristate acetate.

The ability of phorbol myristate acetate (PMA) to induce changes in the expression of B cell surface markers on CR- and CR+ B cells from normal mice in an in vitro culture system was examined. The markers studied were CR, sIgM, sIgD, and sIa. CR- B cells acquired the CR after overnight incubation with PMA. A twofold increase in sIa expression on CR- and CR+ B cells was also noted, whereas the staining intensity of sIgM and sIgD decreased on both B cell populations. These changes in the expression of surface markers took place without detectable increases in cell proliferation, cell size, or RNA content. Furthermore, the same effects were observed when CR- and CR+ B cells were prepared from a small B cell population purified by elutriation. It therefore appears that PMA can exert its effect directly on small, resting B cells.

Animals↗
PubMed1979

[Spontaneous rosette forming, Fc and complement receptor bearing lymphocytes in pediatric diseases].

Investigations with lymphocyte subpopulations were made in 51 children aged from 1-14 years with infections of the upper airways, with acute leukaemias, and other malignant diseases. T-lymphocytes were registered by means of the spontaneous rosette test. The attempt of proving B-lymphocytes was made by means of an EAC test with human erythrocytes, anti-D-immunoglobulins and human complement. The results were compared with those obtained by an EAC test with sheep erythrocytes, sheep haemolysin and mice complement and the significance of complement discussed.

Adolescent↗
PubMed1981

A rapid technique for detecting IgGFc and complement receptors on T and B cells in the neonatally thymectomized and normal adult rat.

Numerous studies have demonstrated the presence of IgGFc and C3 receptors on mammalian lymphoid cells. However, the further characterization of these cells as T, B, or null has been cumbersome and time consuming. A simple method is described for surface fluorescent labeling of (DA X L)F1 rat cell suspensions indirectly with either anti-rat IgM (sIg+) or monoclonal anti-rat thymocyte (sT+) antibody and then rosetting with EA or EAC. Staphylococcus protein A had no significant effect on the level of sIg+ or sT+ attained. From 58-78% of IgGFc+ cells were SIg+ with 14-18% sT+ in the spleen, lymph nodes, and peripheral blood. Almost 100% of C3+ cells were sIg+. Neonatally thymectomized adults exhibited a 254-413% decrease in sT+ cells but a 154-329% increase in sIg+ and a 177-330% increase in null cells. They also exhibited a 140-400% increase in IgGFc+ and C3+ cells in all lymphoid compartments. Fifty-two to 65% of IgGFc+ cells and again almost 100% of C3+ were sIG+. The methods and results are discussed as a basis for studies of B and T lymphocyte maturation and function within various rat lymphoid compartments.

Animals↗
PubMed1975

Ontogeny of Fc and complement receptors in mouse embryonic tissues.

Mouse embryonic tissues were tested for their ability to form rosettes with EA and EAC. It was found that as early as the day after implantation (day 6) a small percentage of cells was able to bind both. After the 8th day of gestation the development of rosette-forming cells paralleled that of the immune system. However, the detection of Fc and C'3 receptors on cells at least 2 days prior to the earliest known demonstration of lymphoid stem cells suggests that they may be expressed on cells other than those of the immune and phagocytic series.

Animals↗
PubMed1978

The nature of the receptor for complement (C3b) in the human renal glomerulus.

The physicochemical nature of the human glomerular complement receptor was studied. Receptor activity was measured by determining the avidity of glomeruli of normal human renal tissue for fluorescein-labeled bacteria (S.typhi) coated with C3b. Maximal binding of C3b-coated bacteria to normal human glomeruli took place in phosphate-saline buffers of pH 6.5 and 0.08 to 0.15 mu ionic strength. Pretreatment of renal tissue with neuraminidase enhanced receptor activity. On the other hand, binding of C3b-coated bacteria to the glomeruli was diminished by pretreatment of the tissue with proteolytic enzymes, phospholipase C and certain lipid solvents. The binding of C3b-coated bacteria to the glomeruli was also diminished by pretreatment of the tissue with fluid-phase C3b, or by pretreatment of the bacteria with C3b inactivator. Normal human serum and purified fluid-phase C3 or the absence of magnesium and calcium ions had little effect on glomerular complement receptor activity.

Binding Sites, Antibody↗
PubMed2005

Human cytomegalovirus downregulates complement receptors (CR3, CR4) and decreases phagocytosis by macrophages.

Human cytomegalovirus (HCMV) infection is associated with an increased susceptibility to opportunistic infections. Although the subversion of adaptive immune responses has been extensively studied, the consequences of HCMV infection on natural immune responses are not well documented. A striking selective downmodulation of CD11b/CD18 (CR3) or CD11c/CD18 (CR4) was found upon HCMV infection, on two models, the monocytic THP-1 cell line and monocyte- derived macrophages. HCMV-infected macrophages have an altered adhesion/phagocytic capacity to Candida albicans, a pathogen responsible for some opportunistic infections in immunocompromised patients. These results suggest a new mechanism implicated in the augmentation of opportunistic infections in HCMV patients.

Candida albicans↗
PubMed2000

Complement receptor 3-like immunoreactivity in the light green cells and the canopy cells of the pond snail, Lymnaea stagnalis.

We observed CR3-like immunoreactivity in the central nervous system (CNS) and its surrounding peripheral nerves of the pond snail, Lymnaea stagnalis. In the CNS of L. stagnalis, the immunoreactivity presenting meshwork-like structure was detected in some neurosecretory cells, which are the light green cells (LGCs) and the canopy cells (CCs), both controlling the body growth. The immunoreactivity was also observed along the edges of median lip nerves. The immunoreactive regions in the median lip nerves appeared to form the axonal plates, from which the LGCs and the CCs release molluscan insulin-related peptides (MIPs) into the blood. By contrast, no immunoreactivity was detected in other neurosecretory cells or their release sites, for example the caudodorsal cells and the cerebral commissure, which release ovulation hormones. The present findings, therefore, suggested that CR3 expresses only in the neurosecretory cells releasing MIPs in L. stagnalis.

Animals↗
PubMed2003

Gonococcal phospholipase d modulates the expression and function of complement receptor 3 in primary cervical epithelial cells.

CR3-mediated endocytosis is a primary mechanism by which Neisseria gonorrhoeae elicits membrane ruffling and cellular invasion of the cervical epithelia. Our data indicate that, upon infection of cervical epithelia, N. gonorrhoeae specifically releases proteins, including a phospholipase D (PLD) homolog, which facilitate membrane ruffling. To elucidate the function of gonococcal PLD in infection of the cervical epithelia, we constructed an N. gonorrhoeae PLD mutant. By comparative association and/or invasion assays, we demonstrated that PLD mutant gonococci are impaired in their ability to adhere to and to invade primary cervical cells. This defect can be rescued by the addition of supernatants obtained from wild-type-infected cell monolayers but not by exogenously added Streptomyces PLD. The decreased level of total cell association (i.e., adherence and invasion) observed for mutant gonococci is, in part, attributed to the inability of these bacteria to recruit CR3 to the cervical cell surface with extended infection. Using electron microscopy, we demonstrate that gonococcal PLD may be necessary to potentiate membrane ruffling and clustering of gonococci on the cervical cell surface. These data may be indicative of the inability of PLD mutant gonococci to recruit CR3 to the cervical cell surface. Alternatively, in the absence of gonococcal PLD, signal transduction events required for CR3 clustering may not be activated. Collectively, our data indicate that PLD augments CR3-mediated gonococcus invasion of and survival within cervical epithelia.

Cells, Cultured↗