About: Complement receptor activity is a research topic. Over the lifetime, 18 publications have been published within this topic receiving 598 citations.
TL;DR: The ability of macrophages to participate in antibody-dependent cell cytotoxicity was reduced dramatically from 2 h after IBR virus infection, suggesting that I BR virus-infected alveolar macrophage undergo alterations in immunological activity long before morphological changes in the cells become apparent.
Abstract: Bovine alveolar macrophages isolated in culture were assessed for immunological activity in assays for Fc and complement receptors, for phagocytosis, and for effector cell function in antibody-dependent cell cytotoxicity. In the case of uninfected alveolar macrophages, Fc receptors were detected on approximately 94% of macrophages and complement receptors were detected on 39%. Phagocytosis of immunoglobulin G-coated sheep erythrocytes occurred in 58% of macrophages, and phagocytosis of opsonized Candida parapsilosis, mediated by the complement receptor, was observed in 68% of cells. Alveolar macrophages were efficient effector cells in antibody-dependent cell cytotoxicity. Infection of macrophages with infectious bovine rhinotracheitis (IBR) virus resulted in reductions in Fc-mediated receptor activity and phagocytosis after approximately 12 and 6 h, respectively. Complement receptor activity was initially elevated and then markedly reduced. Macrophages retrieved from IBR-immune and -susceptible donors were affected to a similar extent. The ability of macrophages to participate in antibody-dependent cell cytotoxicity was reduced dramatically from 2 h after IBR virus infection, suggesting that IBR virus-infected alveolar macrophages undergo alterations in immunological activity long before morphological changes in the cells become apparent.
TL;DR: A highly attenuated vaccine EHV-1 strain also displayed complement receptor activity despite apparent differences of the gp13 gene in restriction enzyme digest pattern and reactivity with monoclonal antibodies, which might contribute to its attenuated phenotype.
TL;DR: There is increase in the numerical expression of CR1 on granulocytes, after asthma provoked experimentally, which is accompanied by increases in granulocyte CR3 after bronchoprovocation with antigen, but not histamine or exercise.
Abstract: Neutrophils demonstrate increased complement receptor activity, measured by rosetting of C3b-coated erythrocytes, after asthma that was provoked experimentally. However, it is not clear whether the increased rosetting is due simply to increase in receptor numbers or whether other factors, such as cell adhesiveness, are involved. We have therefore enumerated granulocyte complement receptors, after asthma provoked experimentally, with monoclonal antibodies against the receptors and flow cytometry. There was a maximal 28.2 +/- 7.5% and 33.4 +/- 9.5% (mean +/- SEM; n = 15) increase in granulocyte CR1 and CR3, respectively, at 3 hours after asthma induced by antigen. There was a maximal 32.0 +/- 7.3% (mean +/- SEM; n = 7) increase in granulocyte CR1, but no change in granulocyte CR3, at 1 hour after exercise-induced asthma. No significant changes in granulocyte CR1 or CR3 were observed up to 6 hours after methacholine challenge, or after exercise in subjects who did not develop exercise-induced asthma. There was a maximal 33 +/- 9% (mean +/- SEM; n = 8) increase in granulocyte CR1 at 30 minutes, but no increase in granulocyte CR3, after histamine challenge of subjects with asthma. Incubation of whole blood with histamine in vitro did not lead to any enhancement in expression of granulocyte CR1. This suggests that antigen- and exercise-induced release of histamine may augment granulocyte CR1 expression through an indirect mechanism. These data indicate that there is increase in the numerical expression of CR1 on granulocytes, after asthma provoked experimentally, which is accompanied by increases in granulocyte CR3 after bronchoprovocation with antigen, but not histamine or exercise.
TL;DR: Cytochemical analysis revealed a consistent, strongly positive reaction for esterase that was sensitive to NaF, and the cytochemical profile of the leukemia cell was similar to that described for LGL.
Abstract: Immunologic, biochemical, and morphologic characteristics of the mononuclear cell from the leukemia of F344 rats were determined. The cells were morphologically similar to large granular lymphocytes (LGL). Surface marker analysis revealed Fc gamma receptors, no Fc gamma receptor or complement receptor activity, and an inability to spontaneously rosette guinea pig erythrocytes. Leukemia cells also had a surface immunoglobulin that hemagglutinated normal rat erythrocytes. The surface immunoglobulin and Fc gamma receptors dissociated from the cell after 2 hours of in vitro incubation, but Fc gamma receptor activity was reexpressed after 6 hours of in vitro incubation. Cells were capable of adherence to glass surfaces but had a low capacity for phagocytosis of latex beads. Cytochemical analysis revealed a consistent, strongly positive reaction for esterase that was sensitive to NaF. The cytochemical profile of the leukemia cell was similar to that described for LGL.
TL;DR: It is postulate that during the acute phase the productive infection of a subpopulation of macrophages that is permissive for LDV results in the synthesis of sufficient interferon to cause activation of the remaining non-permissive macrophage in the animal.
Abstract: Summary
Peritoneal macrophages isolated from Balb/c mice 1 day after infection with lactate dehydrogenase-elevating virus (LDV) exhibited a 5- to 10-fold enhancement of attachment and ingestion of sheep red blood cells coated with immunoglobulin (EAIgG) or immunoglobulin plus complement (EAIgMC). Macrophages isolated from mice 7 days after LDV infection or macrophages infected with LDV in culture were also slightly more active than macrophages from uninfected mice, but the differences were not significant. The results indicate that a specific increase in the number of Fc and C3 receptors on macrophages occurs during the acute phase of infection. This increase correlates with the transient appearance of interferon in acutely infected mice. We postulate that during the acute phase the productive infection of a subpopulation of macrophages that is permissive for LDV results in the synthesis of sufficient interferon to cause activation of the remaining non-permissive macrophages in the animal.