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PubMed1996

Adhesion molecules and IL-1 costimulate T lymphocytes in the autologous MECLR in psoriasis.

Membrane molecules such as CD36 (OKM5), intercellular adhesion molecule-1 (ICAM-1, CD54), gamma interferon-induced protein 10 (gamma-IP10) and IL-1 are induced and/or upregulated in psoriatic epidermis. These molecules have important accessory, trafficking or signalling functions in the immune system and also play a role in the pathophysiology of psoriasis. The relevance of adhesion molecules, CD36 and epidermal IL-1 in psoriasis was studied in vitro in the autologous mixed epidermal cell - T lymphocyte reaction (MECLR). Their level of expression was quantitated in epidermal cell suspensions (ECS) from patients with psoriasis and their function was assessed by blocking with specific mAbs and antisera or by depleting CD36+ cells from the ECS prior to the MECLR. ECS from psoriatic lesions contained increased numbers of CD36+ (23 +/- 12%), ICAM-1(+) (31 +/- 14%) and IL-1(+) (57 +/- 21%) cells. The autologous MECLR was inhibited in samples from all patients by mAb to CD2 (LFA-2), CD11a (LFA-1alpha), CD18 (LFA-1beta), ICAM-1, CD58 (LFA-3) and an antiserum to IL-1beta. Thus, adhesion molecules facilitate inflammation in psoriasis not only via adhesion and recruitment of T lymphocyte in psoriatic lesions, but also via activation of T cells. Furthermore CD36 molecules on psoriatic epidermal cells do not costimulate autologous T lymphocytes in psoriasis. The observed costimulatory function of IL-1beta in the MECLR emphasizes its relevance in psoriasis.

Antibodies, Monoclonal↗
PubMed1991

Mechanisms of serum-enhanced adhesion of human alveolar macrophages to epithelial cells.

Adhesive interactions between macrophages and epithelial cells in the pulmonary alveoli may be important in the pathogenesis of inflammatory lung diseases, such as those induced by cigarette smoking. Potential mechanisms controlling the interactions between these cells were investigated using human alveolar macrophages (AM) and MDCK or A549 epithelial cells. Five percent human serum enhanced the adhesion of AM to MDCK cells by approximately 6-fold and to A549 cells by approximately 1.7-fold. This enhancement was reduced by heating the serum for 30 min at 55 degrees C. Treating normal human serum with methylamine to inactivate C3, substituting C3-deficient serum, or pretreating serum-exposed MDCK cells with anti-C3 F(ab')2 all significantly diminished the adhesion of AM, suggesting that complement is involved. With the use of flow cytometry to examine complement receptors on AM, both CD11b/CD18 and CD11c/CD18 were detected but CR1 was not evident. Preincubating AM with a monoclonal antibody to CD18 reduced the adhesion of AM to MDCK cells by 40% while a significant reduction could not be demonstrated after preincubation with antibodies to either CD11b or CD11c. These data suggest that in the presence of serum C3bi is deposited on the surface of MDCK cells and that AM may attach to these cells, at least in part, through interactions between C3bi and one or more receptors in the CD11/CD18 family, which are present on AM.

Adult↗
PubMed1998

Effect of aprotinin on the red cell immunity in cardiopulmonary bypass.

To investigate the effects of aprotinin on red cell (RC) immune function in the patients undergoing cardiopulmonary bypass (CPB), 20 patients who received valve replacement procedure were prospectively studied. The patients were randomly assigned to aprotinin group and control group. Red blood cell C3b receptor ratio (RC3bRR), red blood cell immune-component ratio (RICR), plasma C3, C4, CH50 and IgG level were determined before operation, at the end of CPB and 1st, 3rd, 7th postoperative days. Our results showed that: (1) The blood requirement was reduced in aprotinin group. (2) After bypass, plasma C3, C4, CH50 was maintained in aprotinin group, while they declined in control group. (3) Plasma level IgG fell in both groups, but at 7th postoperative day it recovered in aprotinin group while the level stayed at low level in control group. (4) The RC3bRR and RICR was mildly inhibited in aprotinin group. It is concluded that the impairment of RC immune function caused by CPB can be mitigated by aprotinin, which may be related to the effects of aprotinin in blood sparing, restriction of complement activation, and reduction of blood requirement which could mitigate the non-specific inflammatory reaction.

Adjuvants, Immunologic↗
PubMed1994

C3b receptor (CR1) genomic polymorphism in rheumatoid arthritis. Low receptor levels on erythrocytes are an acquired phenomenon.

The number of complement receptor 1 (CR1, CD35) molecules on erythrocytes is genetically determined by two codominant alleles. The numerical expression of CR1 on erythrocytes correlates with a HindIII-RFLP or CR1 gene using CR1-1, a complementary DNA probe. We have found low CR1 on erythrocytes in patients with rheumatoid arthritis (RA) in an Indian population. Low levels in RA patients may be acquired or genetically determined. Fifty-two patients with RA, 48 nonrelated healthy subjects and 19 consanguineous relatives of patients were genotyped. CR1 numbers on erythrocytes were quantitated by the enzyme-linked immunosorbent assay using monoclonal anti-CR1 antibody. Normal subjects and patients were followed up for a period of 6 months to evaluate the stability of their CR1 expression. The gene frequency for allele H and L (7.4- and 6.9-kb HindIII restriction fragment, respectively), which correlated with high and low expression of CR1 on erythrocytes was 0.77 and 0.23 in the normal controls. Gene frequency in RA patients was 0.78 and 0.22 for H and L allele, which did not differ significantly from either controls or relatives (0.80 and 0.20 for H and L allele, respectively). However, RA patients expressed fewer CR1 on erythrocytes within each genotype than their relatives and controls. CR1 on erythrocytes were found to be stable in consecutive samples in controls. In RA patients, the number varied between low and high during the course of the disease. The variation in number was significantly correlated (p < 0.05, r = -0.85 to -0.98) with disease activity as monitored by erythrocyte sedimentation rate. Our results suggest that low levels of CR1 on erythrocytes in patients with RA are not inherited, rather they are acquired during the course of the disease.

Adolescent↗
PubMed2004

Effect of lead exposure on the immune function of lymphocytes and erythrocytes in preschool children.

OBJECTIVE: To investigate the influence of lead exposure on the immune function of lymphocytes and erythrocytes in preschool children. MATERIALS AND METHODS: A group of 217 children three to six years of age from a rural area were given a thorough physical examination and the concentration of lead in blood samples taken from each subject was determined. The indices of lymphocyte immunity (CD+3CD+4, CD+3CD+8, CD+4CD+8, CD-3CD+19) and erythrocyte immunity (RBC-C3b, RBC-IC, RFER, RFIR, CD35 and its average fluorescence intensity) of 40 children with blood lead levels above 0.483 micromol/L were measured and compared with a control group. RESULTS: The blood lead levels of the 217 children ranged from 0.11 micromol/L to 2.11 micromol/L. The CD+3CD+4 and CD+4CD+8 cells were lower (P<0.01) and the CD+3CD+8 cells were higher in the lead-poisoned subjects than those in the control group (P<0.05). CD+3 and CD-3CD+19 did not show significant differences. Although the RBC-C3b rosette forming rate was lower and the RBC-IC rosette forming rate was higher in the lead-poisoned group, this difference could not be shown to be statistically significant (P>0.05). RFIR was found to be lower in the lead-poisoned group (P<0.01). Compared with the control group, the positive rate of CD35 was not found to be significantly different in a group of 25 lead-poisoned children (P>0.05), while the average fluorescence intensity was lower in the lead-poisoned group (P<0.05). CONCLUSION: Lead exposure can result in impaired immune function of T lymphocytes and erythrocytes in preschool children.

Child↗
PubMed2003

Vaccinia complement control protein: multi-functional protein and a potential wonder drug.

Vaccinia virus complement control protein (VCP) was one of the first viral molecules demonstrated to have a role in blocking complement and hence in the evasion of host defense. Structurally it is very similar to the human C4b-BP and the other members of complement control protein. Functionally it is most similar to the CR1 protein. VCP blocks both major pathways of complement activation. The crystal structure of VCP was determined a little over a year ago and it is the only known structure of an intact and complete complement control protein. In addition to binding complement, VCP also binds to heparin. These two binding abilities can take place simultaneously and contribute to its many function and to its potential use in several inflammatory diseases, e.g. Alzheimer's disease (AD), CNS injury, xenotransplantation, etc. making it a truly fascinating molecule and potential drug.

Complement Activation↗
PubMed1998

Interleukin-13 increases prostaglandin E2 (PGE2) production by normal human polymorphonuclear neutrophils by enhancing cyclooxygenase 2 (COX-2) gene expression.

OBJECTIVE: To investigate whether interleukin-13 (IL-13) can affect arachidonic acid metabolism and phagocytic activity of normal human polymorphonuclear neutrophils (PMN). METHODS: Normal human PMN (1 x 10(6) cells/ml) were incubated with different concentrations of IL-13 (0.1-10 ng/ml) for a variety of times (30-120 min). Phagocytosis and intracellular cyclooxygenase-2 (COX-2) were detected by flow cytometry. The expression of COX-1 and COX-2 mRNA was detected by RT-PCR. The concentration of PGE2 in the PMN cultured supernatants was determined by EIA. RESULTS: We found that IL-13 at an optimal concentration of 1 ng/ml significantly enhanced COX-2 gene expression and PGE2 production (121.57 +/- 22.17 pg/ml in IL-13 stimulation vs. 73.16 +/- 11.72 pg/ml in controls) by PMN. In addition, IL-13 stimulated PMN phagocytosis via increased complement receptor type 1 (CR1) and type 3 (CR3), but not IgG Fcgamma receptor type 3 (FcgammaRIII). The cytoplasmic neutral esterase activity of PMN was also enhanced by IL-13 stimulation for 24 h. CONCLUSIONS: These results suggest that IL-13 can stimulate PMN and modulates the inflammatory reactions via the cyclooxygenase pathway.

Cells, Cultured↗
PubMed2002

The murine complement regulator Crry: new insights into the immunobiology of complement regulation.

Complement has an important role in inflammation and in the normal function of the immune system. Activated complement fragments have the capacity to bind and damage self-tissues. Cells from vertebrates express on their surface regulators of complement activation that protect them from the deleterious effects of cell-bound complement fragments. Abnormalities in these regulators of complement activation may participate in the pathogenesis of autoimmune diseases and inflammatory disorders. Murine Crry is one of these regulators that inhibits the activation of the third component of complement and protects self-tissues from complement-mediated damage. Experimental work on Crry has increased our understanding of the immunobiology of complement regulation and the potential role of complement and complement inhibitors in the development and treatment of human diseases.

Animals↗
PubMed2000

[The effect of different volume expanders on neutrophil granulocyte function in vitro].

INTRODUCTION: The influence of kolloids on the immune system is not well documented. In this study we investigated the effects of gelatine, hydroxyethylstarch (HES), human albumine, and dextrane on neutrophil function and receptor expression by flow cytometry. METHODS: Whole blood of healthy volunteers was incubated for 30 minutes with either gelatine, HES (6% and 10%), dextrane 40 and 60, or human albumin 20%. Phagocytic capacity was determined by uptake of fluorescein-isothiocyanate labeled bacteria, the conversion of dihydrorhodamine 123 into fluorescent rhodamine 123 was used for oxidative burst measurements. Expression of complement receptors CD 11b and CD35 was investigated using fluorescein-isothiocyanate labeled antibodies. RESULTS: Incubation with gelatine significantly increased expression of complement receptors and oxidative burst. Dextranes and HES had no influence on neutrophil function. Human albumin reduced the oxidative burst, whereas CD 35 expression was increased. CONCLUSION: The physiological significance of these changes in a range of 10% has to be clarified in further investigations.

Bacteria↗
PubMed2005

Extensive genomic and functional polymorphism of the complement control proteins.

Using combinations of genomic markers, we describe more than 20 distinct ancestral haplotypes (AH) of complement control proteins (CCPs), located within the regulators of complement activation (RCA) alpha block at 1q32. This extensive polymorphism, including functional sites, is important because CCPs are involved in the regulation of complement activation whilst also serving as self and viral receptors. To identify haplotypes, we used the genomic matching technique (GMT) based on the pragmatic observation that extreme nucleotide polymorphism is packaged with duplicated sequences as polymorphic frozen blocks (PFB). At each PFB, there are many alternative sequences (haplotypes) which are inherited faithfully from very remote ancestors. We have compared frequencies of RCA haplotypes and report differences in recurrent spontaneous abortion (RSA) and psoriasis vulgaris (PV).

Amino Acid Sequence↗
PubMed2000

The chimpanzee and cynomolgus monkey erythrocyte immune adherence receptors are encoded by CR1-like genes.

The human erythrocyte immune adherence (IA) receptor is the Mr 220,000 type one complement receptor, or CR1. Nonhuman primate IA receptors are comprised of a family of smaller erythrocyte complement receptors (E-CRs) of unknown origin. Recently, the Mr 65,000 baboon E-CR was identified as a glycophosphatidylinositol (GPI)-linked protein encoded by a partially duplicated CR1 gene termed CR1-like. The purpose of this study was to determine the genetic origin of the Mr 75,000 chimpanzee E-CR. Two previously identified cDNAs, an alternative splice product of CR1 termed CR1a and a chimpanzee form of CR1-like, were synthesized and amplified from chimpanzee bone marrow RNA, and transiently expressed in COS-7 cells. By SDS-PAGE, the CR1a protein had a relative mobility slightly greater than chimpanzee E-CR, whereas that of the CR1-like protein was slightly less. Affinity chromatography demonstrated that little chimpanzee CR1a bound to human C3i linked to activated thiol-Sepharose (C3i-ATS), while over 50% of both chimpanzee CR1-like and chimpanzee E-CR bound to C3i-ATS. Treatment with phosphatidylinositol-specific phospholipase C (PIPLC) to assess GPI linkage released E-CR from chimpanzee erythrocytes, and E-CR from cynomolgus monkey erythrocytes. Based on size, ligand-binding specificity, and PIPLC sensitivity, we conclude that the chimpanzee E-CR is encoded by the CR1-like gene. Furthermore, based on PIPLC sensitivity, the cynomolgus monkey E-CR is also likely encoded by a CR1-like sequence. Thus, CR1-like, which is a genetic element of unknown significance in humans, is the gene that encodes the erythrocyte IA receptor of many nonhuman primates.

Amino Acid Sequence↗
PubMed2001

Activated peripheral blood and endothelial cells in thalassemia patients.

BACKGROUND AND OBJECTIVES: Thalassemia patients have alterations in the expression of some activation and adhesion molecules on peripheral blood lymphocytes. We studied cell surface antigens on peripheral blood cells associated with the activation of these cells and soluble molecules produced by activated endothelium. DESIGN AND METHODS: We investigated the expression of CD11b, CD18, CD35, CD43, CD44, and CD69 on the peripheral blood monocytes, Cd11b, CD18, CD35, CD43, CD44, CD67 on peripheral blood neutrophils and CD38 and CD69 on peripheral blood lymphocytes. We studied 68 transfusion-dependent thalassemics (group A), 10 transfusion non-dependent thalassemics (group B), 18 beta-thalassemia carriers (group C), and 28 normal individuals. Relative fluorescence intensity was used to determine the antigen density. Analysis was performed with an EPICS ELITE flow cytometer. Furthermore, soluble intercelullar adhesion molecule 1 (sICAM-1), soluble vascular adhesion molecule 1 (sVCAM-1), and E-selectin, tumor necrosis factor (TNF) alpha, and interleukin (IL) 1beta were measured in the plasma of patients by enzyme-linked immunometric assay. RESULTS: The expression of CD11b, CD18, and CD69 on the monocytes of group A was significantly greater than in groups B and C and in controls, while CD44 was significantly downregulated in group A. CD11b, CD18, CD35, CD44, and CD67 on the surface of neutrophils and CD38 and CD69 on the surface of lymphocytes were also overexpressed in group A. CD44 was downregulated on the monocytes and upregulated on the neutrophils of the patients compared to controls. The levels of sICAM-1, sVCAM-1, E-selectin, TNF-alpha, and IL-1beta in the serum of patients in groups A and B were higher than those in group C and the controls. CONCLUSION: Endothelial activation markers are significantly increased in thalassemia patients, and activated blood cells circulate in the peripheral blood. These may be related to the vascular complications in these patients and might be useful markers for the follow-up of the vascular disease.

Adolescent↗
PubMed2005

Polymorphisms of complement receptor 1 and interleukin-10 genes and systemic lupus erythematosus: a meta-analysis.

A number of studies have tested the association of the complement receptor 1 (CR1) and Interleukin-10 (IL10) polymorphisms with systemic lupus erythematosus (SLE), but reported conflicting results. The aim of the study is to explore whether the CR1 and IL10 genes are associated with SLE susceptibility. We surveyed studies on the CR1 and IL10 polymorphisms and SLE using comprehensive Medline search and review of the references. A meta-analysis was conducted in a fixed effects model or random effects model based on between-study heterogeneity. Eighteen comparisons from 13 studies were included in the CR1 meta-analysis and a total of 16 separate comparisons were used for the IL10 meta-analysis. The CR1 meta-analysis showed no significant association of the CR1 functional polymorphisms with SLE. In contrast, the S structural variant of the CR1 showed a significant association (OR=1.544, 95% CI, 1.217-1.959, P<0.001). Stratification by ethnicity indicated that the CR1 S variant was associated with SLE in Caucasians (OR=1.667, 95% CI, 1.193-2.357, P=0.003). The IL10 meta-analysis showed a significant association between SLE and the G11 allele of IL10.G (OR=1.279, 95% CI; 1.027-1.593, P=0.028) in whole populations, and IL10 promoter -1082G allele was associated with SLE in Asians (OR=1.358, 95% CI; 1.015-1.816, P=0.039). In conclusion, the CR1 meta-analysis revealed the association of the S structural variant of the CR1 with SLE and the IL10 meta-analysis showed the association of IL10.G11 allele and SLE in whole populations and the association between promoter -A1082G polymorphism and SLE in Asians.

Alleles↗
PubMed2000

Expression of complement regulatory proteins in the developing human kidney.

Complement homologous restriction factor CD59 and complement receptor CD35 are typically involved in the regulation of the host defense system. Recent observations in the human fetal kidney suggest a further role for complement cell surface regulators CD35 and CD59 in kidney development and maturation. We investigated this possible role by localizing CD35 and CD59 protein and mRNA in the developing and adult kidney. Adult tissue and fetal tissue ontogeny were analyzed using immunohistochemistry and in situ hybridization. CD35 protein and mRNA were localized to the podocyte of the glomerulus in the human fetal and adult kidney. Expression was initiated after vascularization of the early developing glomerulus. CD59 protein and mRNA were observed as early as 8 weeks' gestation and were localized primarily to the ureteric duct epithelium in the fetal kidney and predominantly to the collecting duct in the adult. Interestingly, CD59 expression was translocated from the basolateral surface in the fetal kidney to the apical surface in the adult kidney. The specific spatial and temporal expression of CD35 and CD59 suggests a possible role for these complement regulatory proteins in renal cell differentiation.

Adult↗
PubMed2002

[Dermatofibrosarcoma protuberans of the breast: a case report].

We describe a dermatofibrosarcoma protuberans (DFSP) of the breast and briefly report about such cases previously mentioned in the literature. A 27-year-old woman was referred because of the progressive increase, during pregnancy, of a mammary nodule located between the internal quadrants of the right breast. Its clinical and radiologic features suggested a fibroadenoma. Lumpectomy revealed a 3-cm, gray-whitish, fasciculated nodule. Histological examination showed a neoplasm characterized by a highly and monomorphic cellular proliferation of spindle-shaped cells, arranged in bundles displaying repetitive storiform growth pattern and infiltrating the adjacent mammary tissue. Lack of necrosis and low mitotic rate was observed. At immunohistochemistry the tumor cells were diffusely positive for vimentin and CD34, but negatively stained with CD99, bc-2, desmin, smooth-muscle actin, S100 protein and cytokeratins. A diagnosis of mammary dermatofibrosarcoma protuberans (DF-SP) was posed. Neoplastic involvement of surgical margins led to a subsequent quadrantectomy without regional lymphadenectomy. The patient was alive and disease-free at the 8-month follow-up. Mammary DFSP is rare. Its preoperative diagnosis is extremely difficult, particularly when radiologic images show an intraparenchymal lesion with round borders. We report such a case and briefly review the pertinent literature. Morphologic parameters to distinguish DFSP from other spindle cell lesions of the breast are discussed.

Adult↗
PubMed2006

Low levels of plasma soluble complement receptor type 1 in patients receiving thrombolytic therapy for acute myocardial infarction.

BACKGROUND: Administration of recombinant soluble CR1 (sCR1) has been shown to attenuate complement mediated myocardial injury in animal models of acute MI. The plasma level of sCR1 in humans with acute MI is not known. We determined the levels of the complement regulatory protein, complement receptor type-1 (CR1) in plasma and its expression on the surface of leukocytes of patients receiving thrombolysis for acute myocardial infarction (AMI). METHODS: Plasma sCR1 was measured by a sandwich ELISA. The levels in patients with AMI were compared with those in normal controls. Leukocyte surface expression of CR1 was measured by flow cytometry. We correlated these parameters with clinical outcome and left ventricular ejection fraction. RESULTS: Patients had very low plasma sCR1 levels. Mean plasma sCR1 levels were significantly less than in controls (6 +/- 3.6 ng/mL vs. 44.6 +/- 12.2 ng/mL, P < 0.00001). Patients who had an adverse in-hospital outcome had significantly lower sCR1 levels when compared to those who had an uneventful course (3.8 +/- 2.0 ng/mL and 7.1 +/- 3.8 ng/mL respectively, P = 0.01). The low plasma sCR1 was despite significantly greater lymphocyte and monocyte surface CR1 (which is a potential source of plasma sCR1). CONCLUSION: Plasma sCR1 levels are reduced in patients receiving thrombolysis for AMI. Replenishing plasma sCR1 might limit complement-mediated injury in this setting.

Adult↗
PubMed1989

Characterization of a monoclonal antibody to guinea pig peritoneal macrophages that inhibits phagocytosis of unopsonized zymosan: structural and functional similarities of the antigen to human and mouse CR3.

A monoclonal antibody, anti-Z-1, was established by fusion of spleen cells from mice immunized with guinea pig thioglycollate-induced peritoneal macrophages (TGC-M phi s) with mouse myeloma cells, P3-X63-Ag8-6.5.3. The Fab' fragments of anti-Z-1 bound to almost all of the TGC-M phi s with a high association constant (6.0 +/- 0.8) X 10(8) M-1, and effectively inhibited phagocytic activities of the cells for unopsonized zymosan and serum-treated zymosan. On the contrary, neither the phagocytic activity for rabbit IgG antibody-sensitized sheep erythrocytes nor that for periodate-treated sheep erythrocytes was inhibited by anti-Z-1. Immunoprecipitation analysis revealed that the antigen recognized by anti-Z-1, which was named Z-1 antigen, consists of a polypeptide chain with a molecular weight of 140,000 (alpha chain) noncovalently associated with a polypeptide chain of 95,000 (beta chain). The epitope with which anti-Z-1 reacts was found to be on the alpha chain by Western blotting. Furthermore, it was found that Z-1 antigen solubilized from the cells with nonionic detergent was capable of binding to unopsonized zymosan, suggesting that Z-1 antigen may function as a receptor for zymosan. These findings show the structural and functional similarities of Z-1 molecules on guinea pig peritoneal macrophages to the third complement receptor on human and mouse leukocytes.

Animals↗