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At least 1,117 records · Page 62Linked to original sources
PubMed1999

Endothelial targeting and enhanced antiinflammatory effects of complement inhibitors possessing sialyl Lewisx moieties.

The complement inhibitor soluble complement receptor type 1 (sCR1) and a truncated form of sCR1, sCR1[desLHR-A], have been generated with expression of the selectin-reactive oligosaccharide moiety, sialyl Lewisx (sLex), as N-linked oligosaccharide adducts. These modified proteins, sCR1sLex and sCR1[desLHR-A]sLex, were assessed in the L-selectin- and P-selectin-dependent rat model of lung injury following systemic activation of complement by cobra venom factor and in the L-selectin-, P-selectin-, and E-selectin-dependent model of lung injury following intrapulmonary deposition of IgG immune complexes. In the cobra venom factor model, sCR1sLex and sCR1[desLHR-A]sLex caused substantially greater reductions in neutrophil accumulation and in albumin extravasation in lung when compared with the non-sLex-decorated forms. In this model, increased lung vascular binding of sCR1sLex and sCR1[desLHR-A]sLex occurred in a P-selectin-dependent manner, in contrast to the absence of any increased binding of sCR1 or sCR1[desLHR-A]. In the IgG immune complex model, sCR1[desLHR-A]sLex possessed greater protective effects relative to sCR1[desLHR-A], based on albumin extravasation and neutrophil accumulation. Enhanced protective effects correlated with greater lung vascular binding of sCR1[desLHR-A]sLex as compared with the non-sLex-decorated form. In TNF-alpha-activated HUVEC, substantial in vitro binding occurred with sCR1[desLHR-A]sLex (but not with sCR1[desLHR-A]). This endothelial cell binding was blocked by anti-E-selectin but not by anti-P-selectin. These data suggest that sLex-decorated complement inhibitors have enhanced antiinflammatory effects and appear to have enhanced ability to localize to the activated vascular endothelium.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1999

Complement receptor 1 (CD35) on human reticulocytes: normal expression in systemic lupus erythematosus and HIV-infected patients.

The low levels of complement receptor 1 (CR1) on erythrocytes in autoimmune diseases and AIDS may be due to accelerated loss in the circulation, or to a diminished expression of CR1 on the red cell lineage. Therefore, we analyzed the expression of CR1 on reticulocytes (R) vs erythrocytes (E). Healthy subjects had a significant higher CR1 number per cell on R (919 +/- 99 CR1/cell) than on E (279 +/- 30 CR1/cell, n = 23), which corresponded to a 3. 5- +/- 1.3-fold loss of CR1. This intravascular loss was confirmed by FACS analysis, which showed that all R expressed CR1, whereas a large fraction of E was negative. The systemic lupus erythematosus (SLE), HIV-infected, and cold hemolytic Ab disease (CHAD) patients had a CR1 number on R identical to the healthy subjects, contrasting with a lower CR1 on their E. The data indicated a significantly higher loss of CR1 in the three diseases, i.e., 7.0- +/- 3.8-, 6.1- +/- 2.9-, and 9.6- +/- 5.6-fold, respectively. The intravascular loss was best exemplified in a patient with factor I deficiency whose CR1 dropped from 520 CR1/R to 28 CR1/E, i.e., 18.6-fold loss. In one SLE patient and in the factor I-deficient patient, the FACS data were consistent with a loss of CR1 already on some R. In conclusion, CR1 is lost progressively from normal E during in vivo aging so that old E are almost devoid of CR1. The low CR1 of RBC in autoimmune diseases and HIV-infection is due to a loss occurring in the circulation by an active process that remains to be defined.

Agglutinins↗
PubMed1999

Ectosomes released by human neutrophils are specialized functional units.

Here we show that human polymorphonuclear leukocytes (PMN) release ectosomes independently of complement attack during their activation both in vitro and at the site of inflammation in vivo. Patterns of biotinylated proteins on the surface of PMN and on PMN-derived ectosomes indicated a specific sorting of cell surface proteins into and out of ectosomes. Ectosomes expressed clusters of complement receptor 1 (CR1), which allowed them to bind efficiently to opsonized bacteria. Myeloperoxidase and human leukocyte elastase, both stored within the azurophilic granules of PMN, were found to colocalize on ectosomes with CR1. Furthermore, myeloperoxidase colocalized with human leukocyte elastase. In contrast, not present on CR1-expressing ectosomes were CD63, a selective marker for the azurophilic granules, and CD14, which is located within the same granules and the secretory vesicles as CR1. Of the other complement regulatory proteins expressed by PMN, only CD59 colocalized with CR1, while CD55 and CD46 were almost absent. Ectosomes released by activated PMN at the site of inflammation may function as a well organized element (ecto-organelle), designed to focus antimicrobial activity onto opsonized surfaces.

Animals↗
PubMed1999

Quantitative alleles of CR1: coding sequence analysis and comparison of haplotypes in two ethnic groups.

The quantitative expression of complement receptor type 1 (CR1) on erythrocytes is regulated by two CR1 alleles that differ in having genomic HindIII fragments of either 7.4 or 6.9 kb and that determine high (H allele) or low (L allele) CR1 expression, respectively, across a 10-fold range. To investigate whether the product of the L allele may contain amino acid substitutions that make it more susceptible to proteolysis, cDNA sequence spanning the CR1 coding region was analyzed in two donors who were homozygous for the H and L alleles and differed by 7-fold in their mean numbers of CR1 per erythrocyte. Sequence differences were detected at 10 nucleotide positions, including 6 that would cause amino acid substitutions. The HindIII RFLP and 3 of the latter 6 sites were analyzed in genomic DNA of 85 Caucasians and 75 African Americans; sites encoding the other amino acid substitutions were analyzed less extensively. Two major haplotypes defined prototypic H and L alleles in both ethnic groups, suggesting that these alleles existed before the African and European populations diverged. Decreased erythrocyte CR1 expression is associated with impaired clearance of immune complexes from blood. Persistence of the L allele in all populations that have been analyzed may suggest a compensatory survival advantage, perhaps related to malaria or another infectious disease.

Alleles↗
PubMed1999

C1q and C4b bind simultaneously to CR1 and additively support erythrocyte adhesion.

Previously, we showed that soluble C1q bound specifically to CR1 on transfected cells. If the CR1-C1q interaction were to participate in immune complex clearance, then this interaction should support E adhesion. Using a tip plate adhesion assay, we found that immobilized C1q mediated adhesion of human E. E binding to C1q was specifically inhibited by polyclonal anti-CR1 Fab fragments. Intact C1 was not efficient as an adherence ligand until it was treated with EDTA or the C1 inhibitor to remove the C1r2C1s2 complex from C1, leaving C1q. Titration of C1q alone, C4b alone, and C1q + C4b indicated that the two complement ligands were additive in their ability to support CR1-mediated adhesion of E. Analysis of binding to immobilized CR1 using a BIAcore instrument documented that C1q, C4b, and C3b binding were independent events. Additionally, C1q-dependent binding of immune complexes and heat-aggregated IgG to E was documented. These experiments confirm that the immune adherence receptor in humans, CR1, is the single receptor for all of the opsonic ligands of complement, provide evidence for a single C1q binding site on LHR-D of CR1, and suggest that C1q may participate in immune clearance.

Antigen-Antibody Complex↗
PubMed1999

Central nervous system-targeted expression of the complement inhibitor sCrry prevents experimental allergic encephalomyelitis.

Although generally thought of as a T cell-driven autoimmune disease, recent studies in experimental allergic encephalomyelitis (EAE), the animal model of multiple sclerosis, suggest a significant role for innate immune mechanisms. To address the possibility that the complement system plays a central role in these diseases, we developed a transgenic mouse with astrocyte-targeted production of a soluble inhibitor of complement activation, complement receptor-related protein y (sCrry). Here, we show that sCrry transgenic mice are either fully protected against EAE or develop significantly delayed clinical signs. These results indicate that complement activation may have an essential role in the pathogenesis of the disease and that complement-mediated events may occur early during the effector phase of EAE. Furthermore, this work underscores the importance of humoral immunity in amplifying a T cell-initiated pathogenic process.

Animals↗
PubMed1998

[The effect of a vaccine made from 39kd hydrophobic outer membrane protein of Leptospira interrogans on neurohumoral and red cell immunity function of the guinea pigs].

A randomized control trial was conducted to determine the immunoprotective efficacy of OmpL39. 36 guinea pigs were divided into OmpL39 group, whole leptospiral cell vaccine (WLCV) group, other proteins of Leptospira group, and negative control group (normal saline, NS). The results showed that all the guinea pigs of infected OmpL39 and WLCV still survived, but all the control guinea pigs died. Immunoprotective efficacy was 100% for OmpL39 and WLCV. OmpL39 levels were similar to WLCV levels and higher than controls (P < 0.05). These suggested that OmpL39 could be used as important immunoprotective antigen to develop the genetic vaccine of the targeting delivery system. Also it was observed that OmpL39 could produce 100% immunoprotective efficacy, have higher MAT level (> 1:3200) and regulate 5-HT, 5-HIAA, DA, NE. The 5-HT, DA, NE concentration was lower and 5-HIAA was higher than that of controls after stimulating the guinea pigs with OmpL39 (P < 0.05). The results suggested that OmpL39 genetic vaccine could produce immunity function and have an active effect on absorbing inflammation and protecting organs and tissues. Besides, the red cell immunity efficacy of the guinea pigs was changed during immunity response and the RBC-C3b RR and the RBC-ICR were increased. The RFER was increased; the RFIR was decreased. RFER/RFIR was remarkably higher than that of control (P < 0.05). These suggested that OmpL39 could increase red cell immunity function.

Animals↗
PubMed1997

[Preliminary study on erythrocyte immunity during sensorineural hearing loss of unknown etiology].

Red cell immune function was determined in 50 patients with sensorineural deafness and 30 healthy persons as control. The results showed that in patients with sensorineural deafness, the red cell C3b receptor (RBC-C3bR) rosette formation rate (15.10 +/- 1.66) was lowered markedly than controls (18.95 +/- 1.16, P < 0.001) and the red cell surface immune complex (RBC-IC 9.94 +/- 1.68) was elevated markedly than controls (7.44 +/- 1.17, P < 0.001). The results indicate that the red cell immunity in the patients with sensorineural deafness of unknown etiology is lowered.

Adolescent↗
PubMed1998

[Influence of insufficient zinc on immune functions in NIDDM patients].

The serum zinc level and immune functions were analyzed in 34 patients with NIDDM before and after the treatment with zinc gluconate supplement during conventional therapy (after the blood glucose level stabilization). The results showed that before treatment the level of serum zinc and red cell C3b receptor rosette(RBCK-C3b RR), T-lymphocyte subgroup CD3, CD4, and CD4/CD8 were decreased(P < 0.01), while CD8, red cell immune complex rosette(RBC-ICR) were increased. After treatment with zinc gluconate for 1 month the serum zinc level, RBC-C3b RR, RBC-ICR, CD3 and CD4/CD8 became normal, CD8 also approached to normal. All the above figures were significantly different before and after zinc therapy. The data showed that various degrees of lowering of serum zinc and abnormal immune functions were present during the conventional antidiabetic therapy. Thus, zinc supplement should be used as an important adjunctive therapy for NIDDM patients.

Adult↗
PubMed2000

EIU in the rat promotes the potential of syngeneic retinal cells injected into the vitreous cavity to induce PVR.

PURPOSE: To determine whether syngeneic retinal cells injected in the vitreous cavity of the rat are able to initiate a proliferative process and whether the ocular inflammation induced in rats by lipopolysaccharide (LPS) promotes this proliferative vitreoretinopathy (PVR). METHODS: Primary cultured differentiated retinal Müller glial (RMG) and retinal pigmented epithelial (RPE) cells isolated from 8 to 12 postnatal Lewis rats were injected into the vitreous cavity of 8- to 10-week-old Lewis rats (10(5) cells/eye in 2 microlieter sterile saline), with or without the systemic injection of 150 microgram LPS to cause endotoxin-induced uveitis (EIU). Control groups received an intravitreal injection of 2 microliter saline. At 5, 15, and 28 days after cell injections, PVR was clinically quantified, and immunohistochemistry for OX42, ED1, vimentin (VIM), glial fibrillary acidic protein (GFAP), and cytokeratin was performed. RESULTS: The injection of RMG cells, alone or in combination with RPE cells, induced the preretinal proliferation of a GFAP-positive tissue, that was enhanced by the systemic injection of LPS. Indeed, when EIU was induced at the time of RMG cell injection into the vitreous cavity, the proliferation led to retinal folds and localized tractional detachments. In contrast, PVR enhanced the infiltration of inflammatory cells in the anterior segment of the eye. CONCLUSIONS: In the rat, syngeneic retinal cells of glial origin induce PVR that is enhanced by the coinduction of EIU. In return, vitreoretinal glial proliferation enhanced the intensity and duration of EIU.

Animals↗
PubMed2000

[Changes of genomic density polymorphism and quantitative expression of complement receptor type 1 in patients with liver diseases].

OBJECTIVE: To study the changes of genomic density polymorphism and quantitative expression of complement receptor type 1 (CR1) on erythrocytes in patients with liver diseases. METHODS: Polymerase chain reaction (PCR) and Hind III restriction enzyme digestion and the quantitative assay of erythrocytic CR1 were used. RESULTS: The spot mutation rate (25.0% approximately 30.3%) of erythrocyte CR1 density gene in patients with liver diseases was not significantly different with that of healthy individuals (28.0%). The amount of erythrocytic CR1 in patients with liver diseases, except for those with normal liver function, was significantly lower than that of healthy individuals (t=10.44, P<0.0001). The quantitative expression of erythrocytic CR1 in decompensated cirrhosis was obviously lower than that of compensated cirrhosis (t=2.21, P<0.05). CONCLUSION: Defective expression of CR1 in liver diseases is acquired through central and/or peripheral mechanisms. It is very important to study the quantitative expression in the evaluation of the development of liver diseases.

Erythrocytes↗
PubMed2000

Complement regulatory proteins and autoimmunity.

To discriminate self from non-self is an essential issue in the immune system. Autologous cells are protected against complement-mediated cell injury by the self-recognition mechanism using complement regulatory proteins composed of complement receptor type 1 (CR1, CD35), membrane cofactor protein (MCP, CD46), decay accelerating factor (DAF, CD55) and homologous restriction factor (protectin, CD59). Recently, the up-regulation of these molecules has been widely shown in inflammatory tissues and organs affected by autoimmune diseases, and in vitro assays have revealed that immune complexes or several cytokines, including interferongamma, tumor necrosis factor alpha, interleukin 1beta and transforming growth factor beta, can up-regulate these molecules. In contrast, it has been found that expression of these complement regulatory proteins is markedly decreased on autologous cells undergoing apoptosis. These findings suggest that complement regulatory proteins have dual roles at inflammatory sites: enhancement of cellular resistance to complement attack and acceleration of the clearance of cells injurious to the organism due to complement-mediated mechanisms. To assist the former function, a therapeutic approach using recombinant soluble complement regulatory proteins may provide a promising strategy for the treatment of autoimmune diseases.

Antigens, CD↗
PubMed2000

Differential expression of surface membrane antigens on bovine monocytes activated with recombinant cytokines and during Trypanosoma congolense infection.

The expression of surface membrane antigens on peripheral blood monocytes (PBM) of cattle of the Boran and N'Dama breeds activated with recombinant cytokines (TNF-alpha and IFN-gamma) and during experimental infection with Trypanosoma congolense was investigated using monoclonal antibodies (MoAbs) and fluorescein-activated cell sorter (FACS). The surface antigens investigated were C3bi receptor, major histocompartibility (MHC) II complex (Ia antigen) and two monocyte/macrophage (Mphi) differentiation antigens. The study revealed that both cytokines caused the enhancement of the expression of all the PBM surface antigens studied. rBolFN-gammaat low concentrations was more efficient in causing the activation of PBM. While the PBM of Boran cattle were more significantly activated to express the C3bi receptor vis-à-vis the Ia antigen than N'Dama cattle, the reverse was the case with the PBM of N'Dama cattle which expressed more Ia antigens than Boran PBM. Similar results were observed during T. congolense infection in the two breeds of cattle. The significantly higher expression of C3bi receptor and correspondingly lower Ia antigen expression by the PBM of Boran cattle, both during trypanosomosis and in vitro may be responsible for the higher rate of erythrocyte phagocytosis, hence the development of more severe anaemia by Boran cattle during trypanosomosis than N'Dama. In addition, the expression of significantly higher numbers of Ia antigen by N'Dama Mphi, hence are more able to process, present and initiate better trypanosome antigen-specific immune response than Boran cattle during infection. These two attributes are known genetic characteristics of trypanotolerance in cattle.

Animals↗
PubMed2000

[CR1 deficiency].

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Complement Activation↗
PubMed1998

[RBC-CR1 genotype polymorphism and RBC immune function in childhood ITP].

OBJECTIVE: To investigate the RBC immune functions in childhood idiopathic thrombocytopenic purpura (ITP). METHODS: RBC-CR1 polymorphism genotype, RBC immune function and its regulator function were detected in 22 ITP, 30 allergic purpura (AP) and 50 normal children by PCR and Guo Feng's method. RESULTS: 1. There were 18 cases of high expression (82%) and 4 of medium expression (18%) of RBC-CR1 genotypes in the ITP cases. The rate of the medium expression genotype was significantly higher in ITP than that in AP and normal children (P < 0.01). 2. The rates of RBC-C3bRR and RBC-C3bRFER were much lower (P < 0.01), and the rates of RBC-ICR and RBC-C3bRFIR were significantly higher in ITP than those in normal children (P < 0.01). 3. RBC-CR1 genotypes in ITP were correlated negatively with RBC-C3bRR and RBC-C3bRFER (P < 0.05), but positively with RBC-ICR and RBC-C3bRFIR (P < 0.05). CONCLUSION: RBC immune participated in the pathogenesis of ITP.

Child↗
PubMed1998

[Studies of tumor necrosis factor-alpha and red cell immunity state in multiple myeloma].

OBJECTIVE: To explore factors in the pathogenesis of multiple myeloma (MM). METHODS: The plasma level of tumor necrosis factor-alpha (TNF alpha) was measured by immunoassay in 21 MM patients, and red cell immunologic function was assayed in 16 patients. RESULTS: There was no difference in TNF alpha levels among patients with either fulminant MM or stable MM and normal controls. The rosette formation rate of red cell C3 bR and red cell immune complex was significantly lower in MM patients than in the controls. CONCLUSION: MM patients might have impaired monocyte-phagocyte system and red cell immune function.

Adult↗