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At least 1,153 records · Page 64Linked to original sources
PubMed1992

Rapid cytokine up-regulation of integrins, complement receptor 1 and HLA-DR on monocytes but not on lymphocytes.

Short-term (3 hr) incubation of whole blood with human recombinant cytokines induced rapid changes in the expression of monocyte but not of lymphocyte surface molecules. The percentage of monocytes bearing CD11b molecules was enhanced by tumour necrosis factor-beta (TNF-beta), whilst that of CD11c was increased by both TNF-alpha and TNF-beta. The mean fluorescence intensity (MFI) of monocyte CD11a was enhanced by interleukin-2 (IL-2), TNF-alpha and TNF-beta, and that of CD11b, CD11c and CD18 was increased by IL-2, IL-4, TNF-alpha and TNF-beta. The proportion of monocytes expressing HLA-DR antigens was not modified by the cytokines investigated, but its MFI was increased by IL-2, IL-4, TNF-alpha and TNF-beta. In contrast, the percentage of monocytes bearing complement receptor 1 (CD35) was enhanced by IL-2, TNF-alpha and TNF-beta but the MFI of this molecule was not modified by these cytokines. The highest up-regulation of CD18, HLA-DR and CD35 was observed with 100 U/ml of either IL-2, IL-4, TNF-alpha or TNF-beta. Decreasing the concentration of all four cytokines from 100 to 10 and 1 U/ml diminished the levels of expression of all molecules, with the exception of CD35, which reached its maximum upon incubation with 1 U/ml of TNF-alpha. IL-1 beta, IL-6 or interferon-gamma (IFN-gamma) did not modify the expression of any of the above monocyte surface determinants. Moreover, none of the lymphocyte surface molecules investigated was modified by 3-hr incubation of blood with cytokines. The demonstration that cytokines selectively and rapidly up-regulate integrins, complement receptor 1 and HLA-DR molecules, on monocytes but not on lymphocytes, suggests that similar mechanisms of mononuclear cell activation by cytokines may control the development and duration of the inflammatory process.

Antigens, CD↗
PubMed1992

Analysis of the effects of activation of the alternative pathway of complement on erythrocytes with an isolated deficiency of decay accelerating factor.

E from individuals with the Inab blood group phenotype have an isolated deficiency of decay accelerating factor (DAF, CD55). DAF is a glycosyl phosphatidylinositol anchored membrane protein that inhibits activation of both the classical and alternative pathways of complement. Deficiency of DAF from the E of paroxysmal nocturnal hemoglobinuria (PNH) is thought to contribute to their greater sensitivity to complement-mediated lysis. Unlike PNH E, however, Inab cells are not susceptible to acidified serum lysis, a process that is mediated through activation of the alternative pathway. This observation led us to hypothesize that membrane constituents other than DAF control susceptibility to acidified serum lysis. To investigate this hypothesis, Inab E were incubated in acidified serum, and hemolysis and C3 deposition (as a measure of alternative pathway activation) were quantitated. C3 deposition of Inab cells was approximately 20 times greater than normal, however, hemolysis was not observed. Inab E expressed a normal amount of membrane inhibitor of reactive lysis (MIRL, CD59), a glycosyl phosphatidylinositol anchored protein that is also deficient in PNH. When MIRL function was blocked with antibody, C3 deposition markedly increased, and 100% of the Inab cells hemolyzed in acidified serum. These studies demonstrate that susceptibility to acidified serum lysis is controlled primarily by MIRL, and that in addition to its regulatory affect on the membrane attack complex, MIRL also modulates the activity of the C3 convertase of the alternative pathway by a mechanism that remains to be determined.

Animals↗
PubMed1992

In vivo binding and clearance of circulating antigen by bispecific heteropolymer-mediated binding to primate erythrocyte complement receptor.

We have used the avidin/biotin system to construct soluble, cross-linked bispecific heteropolymers containing mAb to both the primate E C receptor and the DNP group. These heteropolymers facilitate in vitro binding of DNP-bovine gamma-globulin (DNP-BGG) to both human and squirrel monkey E. Intravenous injection in squirrel monkeys of DNP-BGG followed by heteropolymer leads to E binding and clearance from the circulation of a significant fraction of both heteropolymer and DNP-BGG, without lysis or clearance of the E. This methodology may potentially be used to treat a variety of infectious diseases and other syndromes associated with blood-borne pathogens.

Animals↗
PubMed1992

[Syndrome differentiation in traditional Chinese medicine in chronic aplastic anemia; T-lymphocyte subpopulation in peripheral blood and erythrocyte C3b receptors].

UNLABELLED: In this paper, the Syndrome Differentiation in TCM and the determination on T-lymphocyte subpopulation and RBC C3b receptor were carried out by using indirect SPA assay and RBC C3b receptor ring test among 51 chronic aplastic anemia patients. RESULT: The OKT3, OKT4 and OKT4/OKT8 ratio in groups of Kidney-Yin Deficiency group were lower, while the OKT8 was higher than that of controls. In the group of both Kidney-Yin and Yang Deficiency, OKT4 and OKT4/OKT8 ratio were lower. and the value of OKT8 is higher than that of controls. The OKT8 in the Kidney-Yang Deficiency group was higher. and the ratio of OKT4/OKT8 was lower than that of controls. The OKT8 in the Kidney-Yin Deficiency group among three groups increased higher than that of other two groups. while the OKT4/OKT8 ratio reduced. The OKT4/OKT8 ratio in the group of both Kidney-Yin and Yang Deficiency was higher than that of Kidney-Yang Deficiency group. Among the three groups, the rosette rates of RBC C3b receptor were lower than controls. The above-mentioned data were statistically significant. These characteristic changes could be used as a reference of microcosmic Syndrome Differentiation and also a guide for how to apply the immunosuppressant and immunopotentiator.

Adolescent↗
PubMed1992

[A preliminary study on the red cell immune function in blood stasis syndrome in traditional Chinese medicine].

20 patients with blood stasis syndrome (BSS), 20 patients with non-blood stasis syndrome (NBSS), and 17 normal subjects were measured by tests of RBC-C3b receptor rosette and RBC immune complex rosette. The rates of RBC-C3b receptor rosette formation (RBC-C3b RR, %) in BSS group, NBSS group and normal subjects were 20.90 +/- 4.02, 12.88 +/- 3.29 and 16.74 +/- 4.13 (P less than 0.01) respectively. The rates of RBC immune complex rosette formation (RBC-IC R, %) in the three groups were respectively 8.28 +/- 3.68, 7.73 +/- 2.48 and 7.41 +/- 2.43 (P less than 0.05). RBC-C3b RR was correlated to RBC-IC R in the normal subjects (r = 0.695, P less than 0.001). In patients with the same disease, RBC-C3b RR between the two syndromes (BSS and NBSS) was also very significantly different (P less than 0.01). This study suggested that there are variations on red cell immune function in BSS patients, and also provided an evidence that different syndromes of traditional Chinese medicine exist in diseases.

Adult↗
PubMed1992

Soluble complement receptor type 1 ameliorates the local and remote organ injury after intestinal ischemia-reperfusion in the rat.

We examined the role of C activation in ischemia reperfusion injury by inhibiting C activation in a rat model of mesenteric arterial occlusion. In anesthetized rats, 60 min of mesenteric arterial occlusion was followed by 3 h of reperfusion. PBS alone or containing soluble C receptor 1 (3 or 6 mg) was administered i.v. Controls underwent laparotomy without ischemia. Relative serum C activities were assessed by hemolytic assay, neutrophil (polymorphonuclear leukocyte) sequestration by tissue content of myeloperoxidase (MPO) activity, intestinal mucosal injury by histologic grading, lung vascular permeability by the ratio of bronchoalveolar lavage to blood concentration of radiolabeled BSA, and endothelial cell injury was quantified by measurement of plasma factor VIII-related Ag. After reperfusion, PBS-treated animals had increased intestinal MPO (0.048 +/- 0.007 U/g) compared to sham (0.022 +/- 0.005 U/g (p less than 0.05)) and intestinal mucosal injury score (2.490 +/- 0.221) compared to sham (0.331 +/- 0.045 (p less than 0.05)). Treatment with 6 mg soluble C receptor 1 15 min before reperfusion reduced intestinal MPO (0.017 +/- 0.003 U/g (p less than 0.05)) and mucosal injury (1.733 +/- 0.168 (p less than 0.05)) compared to PBS control. PBS-treated animals also demonstrated increased lung MPO (0.314 +/- 0.025 U/g vs 0.085 +/- 0.018 in sham (p less than 0.05)) and increased lung permeability (bronchoalveolar lavage/blood cpm 11.32 +/- 1.35 x 10(-3) vs sham 2.22 +/- 0.19 x 10(-3) (p less than 0.05)). Treatment with 6 mg soluble C receptor 1 15 min before reperfusion or at reperfusion reduced the lung permeability (bronchoalveolar lavage/blood cpm 3.90 +/- 0.79 x 10(-3) and 5.08 +/- 0.75, respectively (both p less than 0.05)) compared to PBS control, but did not reduce lung MPO (0.342 +/- 0.031 U/g and 0.246 +/- 0.025), respectively. Treatment with sCR1 also reduced the release of factor VIII-related Ag, 5-day mortality, and C hemolytic activity. In this model, C is a major mediator of intestinal injury and extraintestinal injury.

Animals↗
PubMed1992

Cell surface expression of the C3b/C4b receptor (CR1) protects Chinese hamster ovary cells from lysis by human complement.

The C3b/C4b receptor, also known as complement receptor type 1 (CR1, CD35), is a single chain glycoprotein consisting of 30 repeating homologous protein domains known as short consensus repeats (SCR) followed by transmembrane and cytoplasmic domains. A series of recombinant proteins derived from CR1 has been prepared and assessed for the capacity to inhibit complement lysis of the host Chinese hamster ovary (CHO) cells. The full-length recombinant CR1 inhibited human complement-mediated CHO cell lysis, and the efficiency of inhibition was directly proportional to the number of receptors/cell. The SCR 15-18 of CR1, but not SCR 15-16, inhibited complement lysis of the host CHO cell, bound monomeric C3b (Kd,app = 6.5 x 10(-7) M), and dimeric C3b (Kd = 1.8 x 10(-8) M), and served as a cofactor in the proteolysis of C3b by factor I, confirming and extending the observations of Fearon and colleagues (Kalli, K. R., Hsu, P., Bartow, T. J., Ahearn, J. M., Matsumoto, A. K., Klickstein, L. B., and Fearon, D. T. (1991) J. Exp. Med. 174, 1451-1460). The SCR 1-4 of CR1, but not SCR 1-2, also inhibited complement lysis of the host CHO cell, indicating that more than two SCR are necessary and that four SCR are sufficient for optimal C4b binding to CR1. Thus, the structural requirements for C4b binding are analogous to those for C3b binding, namely, four SCR of CR1 form the binding sites for each of these proteins. CR1 has long been recognized to regulate extrinsic complement activation, that is, to bind to and promote the degradation of fluid phase C3b and of C3b attached to immune complex. These results demonstrate that CR1 is also an intrinsic regulator of complement activation in that, under appropriate conditions, CR1 inhibits complement-mediated lysis of the cell on which it is expressed.

Animals↗
PubMed2003

Defective Fc-, CR1- and CR3-mediated monocyte phagocytosis and chemotaxis in common variable immunodeficiency and X-linked agammaglobulinemia patients.

Blood monocyte phagocytic functions were evaluated by chemotaxis, phagocytosis, and superoxide anion production in nine patients with common variable immunodeficiency (CVI), eight patients with X-linked agammaglobulinemia (XLA), and in 17 normal subjects. Further laboratory diagnosis included the determination of the Bruton's tyrosine kinase (Btk) protein expression in monocytes using flow cytometry. The analysis of monocyte phagocytic function demonstrated that CR3-, CR1-, and Fc-mediated phagocytosis (p = 0.0001) were significantly decreased in CVI and XLA patients, and chemotaxis of monocytes (p = 0.0082) was reduced in XLA patients. Superoxide anion production, however, did not differ between the CVI, XLA, and the control groups. The cytoplasmic expression of Btk protein in monocytes was normal in CVI patients and decreased or not detected in XLA patients. It is proposed that impaired chemotaxis and phagocytosis by monocytes may be a characteristic of the innate immune system in CVI and XLA patients, providing a new direction for the physiopathology of these immunodeficiencies.

Adolescent↗
PubMed1992

[The clinical significance of red cell immune adherence function in patients with pulmonary tuberculosis and silicotuberculosis].

In our study, we observed that (1) High RCIA were discovered in these two groups. (2) In the group of pulmonary tuberculosis, the C3b receptor activities remained no change after antituberculous therapy, but the amounts of immune complexes bearing on RBC decreased. In the patients with the high RCIA, CIC was discharged rapidly and the lesions of tissue produced by CIC were prevented. In the patients with silicotuberculosis, both silica and tuberculous bacilli may act as immune adjuvant and enhance the hypersensitivity. So the C3b receptor activities were higher in silicotuberculosis patients.

Adult↗
PubMed1992

Abnormal immune adherence and elimination of hepatitis B surface antigen/antibody complexes in patients with AIDS.

C3b-coated immune complexes (IC) adhere to complement receptor 1 (CR1) on human E in the circulation. E from AIDS patients have an acquired low CR1 number. To study immune adherence and IC elimination in AIDS, radiolabeled hepatitis B surface Ag/antibody complexes were injected i.v. in six AIDS patients and in 14 healthy controls. The binding of IC to E was reduced in AIDS patients (mean binding 2 min after injection: 24.9 +/- 13.3%) compared with healthy individuals (63 +/- 3.7%) (p = 0.0005). The low binding correlated directly with the number of CR1/E and to the capacity of these E to bind IC in vitro. During the first 15 min disappearance of IC was faster in AIDS patients than in normal subjects and correlated with CR1 number. Thereafter, elimination was very slow in AIDS patients, which suggested that a fraction of IC might be released back into the circulation similarly to what has been observed for C3b-coated E. When the data were analyzed with a mathematical model allowing for such release to occur, five of six AIDS patients had a high release rate compared with little or no release in normal individuals (p less than 0.001). Thus, low CR1 on E is responsible for defective immune adherence, and might determine abnormal disappearance of IC from the circulation as well.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Complement receptors in atherosclerotic lesions.

Accumulation of cholesterol in the tunica intima of arteries is a feature of atherosclerotic development. Recently, the demonstration of oxidized LDL in atherosclerotic lesions considerably strengthened the possibility of its role in the atherogenesis in vivo. However, the mechanism of lipid accumulation in monocyte-derived macrophages has not yet been clarified. It has been reported that the complement system may be related to atherosclerosis. In this report, complement receptors in the atherosclerotic lesions obtained from autopsy sample were investigated. Initially C3b receptors were detected using sheep erythrocytes bearing human C3b (EAC1423b cells). EAC1423b cells adherent to only aortic sections showing intimal thickening, but not to intact artery. Second, immunostaining of consecutive aortic sections was performed. Apo B and C5b-9 complex were stained using the indirect immunoperoxidase method, and macrophage, C3b receptor (CR1) and C3bi receptor (CR3) were stained using monoclonal antibody in the alkaliphosphatase anti-alkaliphosphatase method. In the intact artery of 3 month old patient, antigen- specific staining were not observed. In intimal thickening and atheroma of older patients, consecutive sections suggested that complement receptor-expressing cells were macrophages. Staining for apo B antigen existed at extracellular site in the intima, and C5b-9 complex was observed in intima and partially in the media. The above data showed that macrophage complement receptors were expressed in the atherosclerotic lesions when the complement system was activated. We conclude that these data suggest that the complement system and complement receptors may be related to the uptake of LDL by macrophages.

Adolescent↗
PubMed1992

Peripheral blood neutrophils in chronically neutropenic patients respond to granulocyte-macrophage colony-stimulating factor with a specific increase in CR1 expression and CR1 transcription.

Chronically neutropenic patients from a phase I/II protocol were studied for neutrophil (PMN) abnormalities related to therapeutic use of granulocyte-macrophage colony-stimulating factor (GM-CSF). We analyzed phenotype by flow cytometry to measure indirect immunofluorescent staining and activation of transcription by in situ hybridization. PMN count increased in seven of 17 patients. For the group, PMN expression of complement receptors, CR1 and CR3, increased after GM-CSF administration (P less than .005), while expression of class 1 and FcR III was stable. PMN from both of the patients studied by in situ hybridization demonstrated increased expression of CR1 transcript, which in one case coincided in time and intensity with the course of increased CR1 expression, while in the second case the presence of CR1 mRNA increased but lagged behind the increased CR1 protein expression. Thus, PMN activation was observed after GM-CSF infusion, as indicated by increased complement receptor expression. This effect was due both to translocation of receptors from a preformed intracellular pool to the cell surface, and to transcriptional regulation leading to increased receptor synthesis.

Antigens, Surface↗
PubMed2004

[Effects of hypertonic saline on erythrocyte adherence function and bacterial infection of hemorrhagic shock rabbits].

AIM: To explore the effect of hypertonic saline on the erythrocyte adherence function and bacterial infection of hemorrhagic shock rabbits. METHODS: 60 Japanese rabbits were randomly divided into 6 groups, 10 for each group. Artery catheterization and heparin were given to the rabbits in group 1 (sham shock group). Hemorrhagic shock model was set up by bleeding resulting from carotid artery catheter in group 2 (normal saline group )and group 3 (hypertonic saline group). 30 minutes after shock, the rabbits in group 1 and group 2 were treated with normal saline and balanced salt solution containing 1 x 10(9)/kg E.coli, respectively. And the rabbits in group 3 were treated with 75 g/L NaCl solution and balanced salt solution containing 1 x 10(9)/kg E.coli. Then the survival rates of the rabbits in group 1-3 were observed. Rabbits in group 4-6 were same treatment as received, group 1-3, respectively, except that there was no E.coli in balanced salt solution. The erythrocyte immune adherence function of rabbits in group 4-6 were detected 5 hours after shock by RBC-C3bR and RBC-IC rosette forming assays. RESULTS: The survival rate of rabbits in hypertonic saline group was significantly higher than that in normal saline group. The RBC-C3bR rosette forming rate of the normal saline treated rabbits were pronouncedly decreased, while RBC-IC rosette forming rate was notably elevated, as compared with those of either sham shock group or hypertonic saline group(P<0.01). Hypertonic saline markedly increased RBC C3bR rosette forming rate. CONCLUSION: The above findings suggest that hypertonic salt solution can remarkably improve the depressed erythrocyte immune adherence function and enhance the rabbit's resistance to E.coli challenge after hemorrhagic shock.

Animals↗
PubMed2005

[Effects of Eupolyphaga Sinensis Walker on erythrocyte's CR1 activity and anti-cardiolipin antibody level in rats with stagnation of blood].

AIM: To study the effect of Eupolyphaga Sinensis Walker(ESW) on red blood cell immune adherence (RCIA) and serum anticardiolipin antibody level in rat model of Yin-deficiency Huo-excess with chronic blood stasis. METHODS: The model was made by i.m. injection of dexamethasone (0.5 mg/kg) and adrenaline (0.84 mg/kg). The serum anti-cardiolipin antibodies (ACA) ACA-IgG, ACA-IgA and ACA-IgM and the plasma D-dimmer levels were measured by using enzyme-linked immunosorbent assay (ELISA). The body and organ weight of the rats were measured. RESULTS: For rats of Yin-deficiency Huo-excess, rosette rates of red blood cell C3b receptors (RBC-C3b RR) and red blood cell cancer (RBC-CaR) decreased, the serum ACA-IgG, ACA-IgA, ACA-IgM and the plasma D-dimmer levels markedly increased, body weight and the weight of spleen and thymus all decreased. ESW (5 mg/kg, 10 mg/kg) increased RBC-C3bRR and RBC-CaR, reduced serum ACA-IgG, ACA-IgA, ACA-IgM and plasma D-dimmer levels, and increased spleen weight of the rats. CONCLUSION: ESW can boost the immune function in rats of Yin-deficiency Huo-excess with chronic blood stasis.

Animals↗