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PubMed2001

Molecular identification of Knops blood group polymorphisms found in long homologous region D of complement receptor 1.

Complement receptor 1 (CR1) has been implicated in rosetting of uninfected red blood cells to Plasmodium falciparum-infected cells, and rosette formation is associated with severe malaria. The Knops blood group (KN) is located on CR1 and some of these antigens, ie, McCoy (McC) and Swain-Langley (Sl(a)), show marked frequency differences between Caucasians and Africans. Thus, defining the molecular basis of these antigens may provide new insight into the mechanisms of P falciparum malaria. Monoclonal antibody epitope mapping and serologic inhibition studies using CR1 deletion constructs localized McC and Sl(a) to long homologous repeat D of CR1. Direct DNA sequencing of selected donors identified several single nucleotide polymorphisms in exon 29 coding for complement control protein modules 24 and 25. Two of these appeared to be blood group specific: McC associated with K1590E and Sl(a) with R1601G. These associations were confirmed by inhibition studies using allele-specific mutants. A sequence-specific oligonucleotide probe hybridization assay was developed to genotype several African populations and perform family inheritance studies. Concordance between the 1590 mutation and McC was 94%; that between Sl(a) and 1601 was 88%. All but 2 samples exhibiting discrepancies between the genotype and phenotype were found to be due to low red cell CR1 copy numbers, low or absent expression of some alleles, or heterozygosity combined with low normal levels of CR1. These data further explain the variability observed in previous serologic studies of CR1 and show that DNA and protein-based genetic studies will be needed to clarify the role of the KN antigens in malaria.

Animals↗
PubMed2001

Newly recognized cellular abnormalities in the gray platelet syndrome.

The gray platelet syndrome (GPS) is a rare congenital bleeding disorder in which thrombocytopenia is associated with increased platelet size and decreased alpha-granule content. This report describes 3 new pediatric cases presenting with the classical platelet abnormalities of GPS within one family with normal parents. Examination of blood smears of the 3 patients demonstrated not only gray platelets, but also gray polymorphonuclear neutrophils (PMNs) with decreased or abnormally distributed components of secretory compartments (alkaline phosphatase, CD35, CD11b/CD18). Secondary granules were also decreased in number as assayed by immunoelectron microscopy. These data confirm that the secretory compartments in neutrophils were also deficient in this family. Megakaryocytes (MKs) were cultured from the peripheral blood CD34+ cells of the 3 patients for 14 days, in the presence of thrombopoietin and processed for immunoelectron microscopy. Although von Willebrand factor (vWF) was virtually undetectable in platelets, vWF immunolabeling was conspicuous in cultured maturing MKs, particularly within Golgi saccules, but instead of being packaged in alpha-granules, it was released into the demarcation membrane system. In contrast, P-selectin followed a more classical pathway. Double-labeling experiments confirmed that vWF was following an intracellular pathway distinct from the one of P-selectin. In these 3 new cases of GPS, the MKs appeared to abnormally process vWF, with secretion into the extracellular space instead of normal alpha-granule packaging. Furthermore, the secretory compartment of another blood cell line, the neutrophil, was also affected in this family of GPS.

Alkaline Phosphatase↗
PubMed2002

Crry, but not CD59 and DAF, is indispensable for murine erythrocyte protection in vivo from spontaneous complement attack.

Decay-accelerating factor (DAF) and CD59 are 2 glycosylphosphatidylinositol-anchored membrane proteins that inhibit complement activation at the C3 and C5b-9 step, respectively. CD59 is considered critical for protecting erythrocytes from spontaneous complement attack, as deficiency of CD59 or CD59/DAF, but not of DAF alone, on human erythrocytes renders them sensitive to complement lysis in paroxysmal nocturnal hemoglobinuria syndrome. To evaluate the relative roles of CD59 and DAF in vivo, we have generated and studied a CD59 knockout and a CD59/DAF double-knockout mouse. CD59-deficient and CD59/DAF-double-deficient mouse erythrocytes were highly sensitive to antibody-induced complement lysis in vitro, yet neither CD59 knockout nor CD59/DAF double-knockout mouse developed spontaneous hemolytic anemia. Consistent with the latter observation, erythrocytes from the 2 strains of mutant mice were shown to have a normal lifespan in vivo. In contrast, mouse erythrocytes deficient in complement receptor 1 (CR1)-related gene y (Crry), a membrane C3 inhibitor with DAF and membrane cofactor protein activities, were rapidly eliminated from the circulation by a complement-dependent mechanism. Compared with DAF-deficient erythrocytes, Crry-deficient erythrocytes incurred higher levels of spontaneous C3 deposition in vivo. These findings demonstrate that CD59 and DAF are not indispensable on murine erythrocytes. Rather, effective C3 regulation on the cell surface, provided by Crry rather than DAF, is necessary for mouse erythrocytes to resist spontaneous complement attack. Our results raise the possibility that proper control of C3 activation may also be critical on human erythrocytes, where CR1 but not DAF could be the principal regulator of spontaneous C3 activation.

Animals↗
PubMed2003

Endothelial cells modulate eosinophil surface markers and mediator release.

Migration from blood to tissue modulates eosinophil function, possibly through interactions with endothelial cells. The effects of contact with and migration through endothelial cells on eosinophil expression of surface markers and release of leukotriene C4 were evaluated. A small proportion (2.6%) of eosinophils spontaneously migrated through endothelial cell monolayers. Activation of endothelial cells by interleukin (IL)-4 or IL-1beta slightly increased this migration (to 12.4%), which became much greater when a chemoattractant was placed in the lower chamber (84.3%). However, the chemotactic effect was downregulated by pretreating endothelial cells with interferon gamma (IFN-gamma; 63.1%). At baseline, 5% of eosinophils expressed CD69; this increased to 30.7% in culture on untreated endothelial cells and to 50.9% on IL-1beta-pretreated endothelial cells. This effect was mediated through intercellular adhesion molecule-1/CD11b interaction. Eosinophil migration through endothelial cells further increased CD69 expression to 63.9% and also increased CD35 expression from 83.3 to 91.3%. Upon stimulation, eosinophils that had migrated through endothelial cells produced more leukotriene C4 than control cells (872.4 and 103.9 pg x mL(-1), respectively). Endothelial cell pretreatment with IL-4 or IL-1beta further increased leukotriene C4 release (1,789.1 and 2,895.1 pg x mL(-1), respectively), whereas pretreatment with IFN-gamma decreased it (293.7 pg x mL(-1)). These data show that in vitro interactions with endothelial cells upregulate eosinophil membrane receptor expression and mediator release and that these effects are differently modulated by T-helper cell type 1 and 2 cytokines. These eosinophil modulations may play an important role in asthma pathogenesis.

Adjuvants, Immunologic↗
PubMed1998

Soluble complement receptor type 1 (CD35) in bronchoalveolar lavage of inflammatory lung diseases.

Complement receptor type 1 (CR1) (CD35; C3b/C4b receptor) is a transmembrane protein of many haematopoietic cells. Once cleaved, soluble complement receptor type 1 (sCR1) exerts opposite effects as a powerful inhibitor of complement. This study addressed both the question of whether sCR1 was found in bronchoalveolar lavage (BAL) of normals and patients with various inflammatory disease, and its possible origin. In this retrospective study covering specimen and clinical data of 124 patients with acute and chronic inflammatory lung pathologies, BAL supernatants were analysed by enzyme-linked immunosorbent assay technique for sCR1. Correlations were made between the sCR1 levels obtained and the constituents of BAL. Human alveolar macrophages were cultivated in order to determine their secretory capacity of sCR1. Alveolar macrophages from normal subjects were shown to release sCR1 in vitro. In addition, sCR1 was present in BAL of normal controls and was significantly increased in acute inflammatory lung diseases such as acute respiratory distress syndrome (ARDS), bacterial and Pneumocystis carinii pneumonia, as well as in chronic inflammatory diseases such as interstitial lung fibrosis and sarcoidosis. In BAL of ARDS, bacterial, and P. carinii pneumonia, there was a good correlation between sCR1 and the absolute neutrophil counts. In sarcoidosis, a correlation was found with BAL lymphocyte counts. Serum sCR1 was not increased in patients compared to controls. Soluble complement receptor type 1 (sCR1) is found in the bronchoalveolar lavage in health as well as in acute and chronic inflammatory disease. Alveolar macrophages are capable of releasing sCR1 in vitro and may be the main physiological source of sCR1 in the alveoli. The good correlation between sCR1 and the absolute neutrophil or lymphocyte numbers in bronchoalveolar lavage of inflammatory diseases suggests a predominant role of leucocytes for the release of sCR1 in such conditions. The release of this inhibitor of complement may be crucial to control and reduce complement activation and thus prevent lung injury.

Bronchoalveolar Lavage Fluid↗
PubMed2005

Follicular dendritic-like cells derived from human monocytes.

BACKGROUND: Follicular dendritic cells (FDCs) play a central role in controlling B-cell response maturation, isotype switching and the maintenance of B-cell memory. These functions are based on prolonged preservation of antigen and its presentation in its native form by FDCs. However, when entrapping entire pathogens, FDCs can turn into dangerous long-term reservoirs that may preserve viruses or prions in highly infectious form. Despite various efforts, the ontogeny of FDCs has remained elusive. They have been proposed to derive either from bone marrow stromal cells, myeloid cells or local mesenchymal precursors. Still, differentiating FDCs from their precursors in vitro may allow addressing many unsolved issues associated with the (patho-) biology of these important antigen-presenting cells. The aim of our study was to demonstrate that FDC-like cells can be deduced from monocytes, and to develop a protocol in order to quantitatively generate them in vitro. RESULTS: Employing highly purified human monocytes as a starter population, low concentrations of Il-4 (25 U/ml) and GM-CSF (3 U/ml) in combination with Dexamethasone (Dex) (0.5 microM) in serum-free medium trigger the differentiation into FDC-like cells. After transient de-novo membrane expression of alkaline phosphatase (AP), such cells highly up-regulate surface expression of complement receptor I (CD35). Co-expression of CD68 confirms the monocytic origin of both, APpos and CD35pos cells. The common leukocyte antigen CD45 is strongly down-regulated. Successive stimulation with TNF-alpha up-regulates adhesion molecules ICAM-1 (CD54) and VCAM (CD106). Importantly, both, APpos as well as APneg FDC-like cells, heterotypically cluster with and emperipolese B cells and exhibit the FDC characteristic ability to entrap functionally preserved antigen for prolonged times. Identical characteristics are found in monocytes which were highly expanded in vitro by higher doses of GM-CSF (25 U/ml) in the absence of Dex and Il-4 before employing the above differentiation cocktail. CONCLUSION: In this work we provide evidence that FDC-like cells can be derived from monocytes in vitro. Monocyte-derived FDC-like cells quantitatively produced offer a broad utility covering basic research as well as clinical application.

Alkaline Phosphatase↗
PubMed2005

Complement regulatory protein Crry/p65-mediated signaling in T lymphocytes: role of its cytoplasmic domain and partitioning into lipid rafts.

Crry/p65 is a type I glycoprotein, which protects mouse T cells from complement attack. We have previously shown that complement receptor I-related protein Crry/p65 (Crry) ligation has a costimulatory effect on mouse CD4+ T cell activation. Here, we have examined the mechanisms responsible for Crry costimulation, addressing the question of whether Crry potentiates signal transduction starting at the T cell receptor (TCR)/CD3 complex or promotes distinct costimulatory signals. We show that Crry increases early TCR-dependent activation signals, including p56lck-, zeta-associated protein-70 (ZAP-70), Vav-1, Akt, and extracellular signal-regulated kinase (ERK) phosphorylation but also costimulation-dependent mitogen-activated protein kinases (MAPK), such as the stress-activated c-Jun N-terminal kinase (JNK). It is intriguing that Crry costimulus enhanced p38 MAPK activation in T helper cell type 1 (Th1) but not in Th2 cells. A fraction of Crry is found consistently in the detergent-insoluble membrane fraction of Th1 or Th2 cells or CD4+ lymphoblasts. Crry costimulation induced clustering of lipid rafts, increasing their content in Crry, CD3epsilon, and p59-60 forms of p56lck, and caused actin polymerization close to the site of activation in Th2 cells. Such events were inhibited by wortmannin, suggesting a role for phosphatidylinositol-3 kinase in these effects. The Crry cytoplasmic domain was required for JNK activation and interleukin-4 secretion but not for the presence of Crry in rafts or activation of p56lck, ZAP-70, Akt, Vav-1, or ERK. This suggests that Crry costimulation involves two different but not mutually exclusive signal transduction modules. The dual function of Crry as a complement regulatory protein and as a T cell costimulator illustrates the importance of complement regulatory proteins as links between innate and adaptive immunity.

Animals↗
PubMed2004

Modulation of urinary CR1 in systemic lupus erythematosus.

The decline in the levels of erythrocyte complement receptor 1 (ECR1) in systemic lupus erythematosus (SLE) has been widely reported. The most probable cause for this decline is excessive proteolytic shedding of CR1 from the cell surface. Similarly a decline in glomerular CR1 (GCR1) has also been reported in SLE. Because CR1 is excreted in urine it is imperative to study the relationship of urinary CR1 (uCR1) with ECR1 and GCR1, and their overall correlation with disease activity. We have determined the levels of uCR1, ECR1 and GCR1 in SLE patients and compared them with normal controls and minimal change disease (MCD) patients. We found a significant decline in both uCR1 and GCR1 in SLE but not in MCD; levels of uCR1 in MCD were either comparable to those of controls or higher. Immunofluorescence for GCR1 was very high in MCD. We did not find any correlation between ECR1, uCR1 and kidney function tests on divariate scatter analyses. The correlation coefficient for uCR1 and GCR1 was highly significant and positive. Our findings thus suggest that uCR1 reflects the levels of GCR1 expression, which decline drastically in SLE. Therefore we envisage uCR1 as a potential marker for glomerular involvement in SLE.

Case-Control Studies↗
PubMed1987

Impaired surface membrane expression of C3bi but not C3b receptors on neonatal neutrophils.

Because increased complement receptor expression is necessary for optimal function of adult neutrophils, we tested the hypothesis that the increased susceptibility of neonates to infection might be due to an impaired ability of neonatal neutrophils to increase expression of complement receptors in response to chemotactic stimuli. We used monoclonal antibodies and flow cytometry to compare surface expression of the receptors for the complement components C3b (CR1) and C3bi (CR3) on adult and neonatal cord blood neutrophils (PMNs). We also compared receptor expression on PMNs from infants delivered by cesarean section without labor versus infants delivered vaginally. Expression of both CR1 and CR3 was minimal on resting adult and neonatal PMNs maintained at 0 degrees C. There was a modest increase in expression of both receptors when PMNs were warmed to 37 degrees C. This increase was similar on adult and neonatal cells, both unfractionated in whole blood and after isolation with Percoll density centrifugation, with one exception. Expression of CR1 was greater on isolated PMNs from vaginally delivered infants versus adults when the cells were warmed to 37 degrees C. This difference was not observed with cells from infants delivered by cesarean section without labor, suggesting this modest increase in receptor expression may be due to factors associated with labor. When isolated cells were stimulated with either N-formyl-methionyl-leucyl-phenylalanine or zymosan-activated serum, expression of CR1 increased to the same extent in both neonatal and adult PMNs. In contrast, maximal CR3 expression on cord PMNs stimulated with N-formyl-methionyl-leucyl-phenylalanine or zymosan-activated serum was only 75% of the adult values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Fluorescent cytometric analysis of polymorphonuclear leukocytes in Chediak-Higashi syndrome: diminished C3bi receptor expression (OKM1) with normal granular cell density.

Chediak-Higashi Syndrome (CHS) has been associated with recurrent bacterial infections and defective polymorphonuclear (PMN) leukocyte function. Confirmation of the diagnosis of CHS and defective PMN function was established in a 2-month-old with accelerated phase CHS. The diagnosis was confirmed by demonstrating reduced PMN degranulation (beta-glucuronidase release 34.1 +/- 0.9% versus 5.1 +/- 4% and lysozyme release 17.6 +/- 1.2% versus 11.1 +/- 7% (control versus CHS) and staphylococcal bacterial killing at 15' 51.4 +/- 3.6% versus 24.9 +/- .4% (control versus CHS). Additional studies using fluorescent cytometric analysis were made to investigate other etiologies of PMN dysfunction in CHS. Total cell density and PMN granularity, as measured by fluorescent-activated cell sorter side scatter analysis, was no different from CHS and age-matched controls. Although CHS is characterized by large PMN granular inclusions, right angle light scatter analysis in this study suggests that the total cell density within the PMN of patients with CHS is normal (D less than .01). PMN granular release of surface receptors was also studied using antibody binding and fluorescent analysis. OKM1 antibody-binding demonstrated significantly reduced C3bi (MO-1) receptor expression (13% of control) p less than 0.001. Decreased surface reception expression of C3bi receptors may play an additional role in defective PMN mobility, chemotaxis, and bactericidal activity in patients with CHS.

Antibodies, Monoclonal↗
PubMed1993

Lipid and membrane protein transfer from human neutrophils to schistosomes is mediated by ligand binding.

Attachment of human neutrophils to schistosomula of Schistosoma mansoni involves leukocyte receptors recognizing carbohydrate, complement and/or IgG ligands on the parasite surface. Here, we examined the transfer of a fluorescent fatty acid analog (BOFA) from human neutrophils to schistosomula coated with concanavalin A (Con A), immune serum or nonimmune serum under co-culture conditions by fluorescence confocal laser scanning microscopy (CLSM). Coating schistosomes with Con A or immune serum and co-culturing them for 24 hours with BOFA-labeled neutrophils resulted in a specific lipid transfer to the surface tegument of the schistosomes. Tegumental labeling was absent when nonimmune serum was used. No significant difference (P < 0.001) was found in the number of neutrophils bound to the worm surface between Con A-coated schistosomes (4.1 +/- 0.345 cells/worm) and worms incubated in immune serum (4.261 +/- 0.362). The number of neutrophils bound to the schistosomula (2.7 +/- 0.223) was significantly reduced in the presence of nonimmune serum (P < 0.0001). The viability of the schistosomula was 98% in nonimmune treated co-cultures, and 91% in cocultures treated with immune serum. HPLC analysis of labeled neutrophils demonstrated that BOFA was incorporated into both phospholipids and neutral lipids, which were almost exclusively triglycerides and, after 18 hours of culture, all of the fatty acid analog was incorporated into complex lipids. Double-label experiments in which schistosomula bearing Con A were first incubated with BOFA-labeled neutrophils and subsequently immunolabeled revealed that the neutrophil membrane proteins, MHC class I, CR1 and CR3 were co-transferred with neutrophil lipids to the parasite tegument.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

C3 receptors on macrophages.

The complement receptors on macrophage are responsible for their binding and ingestion of opsonized targets. The two established receptors are CR1, which recognizes C3b, and CR3, which recognizes iC3b, the natural product of C3b from cleavage by the complement control protein factor I and its cofactors. CR1 belongs to a group of proteins that contain a structural element characterized by its size of 60-65 amino acids, and four conservatively positioned cysteines, which engage in a self-contained 1-3, 2-4 disulphide arrangement. This structural unit is called SCR (short consensus repeat) and is found in the complement proteins C1r, C1s, C2, factor B, factor H, C4BP, DAF, MCP and CR2, each of which interacts with some cleavage products of C3 and/or C4. CR1 has 30 SCR units accounting for its entire extracellular structure. It has a transmembrane segment and a small cytoplasmic domain. CR3 is a heterodimer containing an alpha and beta subunit held together by non-covalent forces. The beta subunit is also found in the two leukocyte antigens, LFA-1 and p150,95, which have alpha subunits distinct from that of CR3. The beta subunit contains 56 cysteine residues, 42 of which lie in a span of 256 residues immediately adjacent to the transmembrane segment. It shares extensive sequence homology with subunits of membrane protein complexes that bind fibronectin and vitronectin, implicating that they all belong to an extended set of surface adhesion molecules not restricted to the immune system. p150,95 is also expressed on macrophages and it has iC3b binding activity. It also shares some functional properties with CR3 as an adhesion surface molecule.

Chemical Phenomena↗
PubMed1994

Serum biochemical changes and chemiluminescent responses of whole blood in Holstein cattle with leukocyte adhesion deficiency.

Serum biochemical profile and whole blood chemiluminescent (CL) responses in 8 Holstein cattle affected with leukocyte adhesion deficiency (LAD) were evaluated. Concentrations of sodium, chloride and calcium in serum from cattle affected with LAD were significantly (p < 0.05) decreased as compared with controls. The characteristic changes in serum proteins were hypoalbuminemia and hyperglobulinemia, and the concentrations of albumin and gammaglobulin in serum from normal cattle and cattle affected with LAD were significantly (p < 0.01) different. Significantly (p < 0.01) diminished CL indices and prolonged peak time of CL responses in whole blood were detected in cattle affected with LAD. These findings indicate that the CL response associated with iC3b receptor mediated phagocytic activity is impaired in cattle affected with LAD. The whole blood CL assay appeared to be practical and useful for routine evaluation of blood samples from cattle affected with LAD.

Animals↗
PubMed2004

CR1-based inhibitors for prevention of complement-mediated immune hemolysis.

Complement receptor 1 (CR1) is a single pass transmembrane glycoprotein that, through its ability to bind key components of the complement cascade, can inhibit both the classical and alternative pathways. Using several animal models, a recombinant form of CR1 has been documented to be effective in reducing tissue damage that occurs as a result of complement activation in various inflammatory conditions. This strategy is currently being explored in human clinical trials. Activation of complement cascade via the antibody-mediated classical pathway can initiate red blood cell destruction, causing transfusion reactions and hemolytic anemia. We discuss here our approach of using CR1 derivatives as therapeutic targets for prevention of complement-dependent immune hemolysis. Using a mouse model of hemolytic transfusion reaction, we have found that sCR1 treatment reduces complement activation and prolongs the survival of transfused red blood cells. Through structure-function analysis, we have identified a complement inhibitory domain located at the amino-terminal region of CR1 that mediates its antihemolytic activity in vivo. Collectively, our data highlight a potential use for CR1 to control complement-dependent immune hemolysis and identify its functional domains for the future design of CR1-based inhibitors.

Anemia, Hemolytic↗
PubMed2005

Complement regulation during pregnancy.

Complement has an important role in innate immunity and inflammation. Complement also has the capacity to attack self tissues. Cells are protected from the deleterious effects of complement. The Crry protein belongs to a family of molecules that regulates complement activation, protecting tissues from complement-mediated damage. To investigate the role of these molecules in vivo, Crry-/- mice were generated. Crry-/- mice did not survive pregnancy owing to abnormal complement deposition in the placenta through the alternative pathway. Tissue damage related to C5 (production of C5a and C5b-9) was not required. Removal of inflammatory cells did not affect the phenotype. This suggests new noninflammatory mechanisms of pregnancy failure that are dependent solely on C3. The major abnormality was a failure of blood vessel formation in the placenta, revealing an unsuspected C3 effect in the vascular development of this organ.

Animals↗
PubMed1990

Altered erythrocyte CR1 binding kinetics compensate for decreased binding capacity in rheumatoid arthritis.

Patients with rheumatoid arthritis have decreased numbers of CR1 per erythrocyte and decreased binding of immune complexes to erythrocytes. Overall erythrocyte immune complex binding activity depends on both the number and the binding kinetics of CR1. We measured kinetic parameters for the interaction between a complement-containing dsDNA:anti-dsDNA probe and erythrocytes in patients with rheumatoid arthritis and normal controls. The results indicate that: 1) the maximum quantity of immune complexes bound per erythrocyte was significantly decreased in rheumatoid arthritis compared with normal controls (p less than or equal to 0.009); 2) the steady state binding constant, Kss, and the association rate constant for binding of immune complexes to erythrocytes, ka, were significantly increased in rheumatoid arthritis versus normal controls (p less than or equal to 0.0001 and 0.002 respectively); 3) the dissociation rate constant for the release of bound immune complexes from erythrocytes, kd, was slightly smaller in rheumatoid arthritis but this difference was not statistically significant; and 4) the energies of activation for the association and dissociation reactions, Eaa, and Ead, did not differ between the two groups. These data confirm that while the maximum quantity of immune complexes bound per erythrocyte is decreased in rheumatoid arthritis, the association rate constants are larger and dissociation rate constants slightly smaller than those of normal controls. Changes in these kinetic parameters compensate for the decrease in the maximum quantity of immune complexes bound per erythrocyte.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigen-Antibody Complex↗
PubMed2004

Intramyocardial CD34+ cell transplantation combined with off-pump coronary artery bypass grafting.

This report describes a new therapeutic approach for severe ischemic heart disease, intramyocardial transplantation of autologous bone marrow-derived CD34 + cells combined with off-pump coronary artery bypass grafting (CABG). CD34 is widely known as a cell surface antigen expressed on hematopoietic stem cells, and recent experimental studies have shown that CD34 + cells include endothelial progenitor cells. We used the Isolex 300i magnetic cell selection system to separate CD34 + cells from bone marrow cells. This report describes the first case treated with the combination of off-pump CABG and cell transplantation for therapeutic angiogenesis and myocardial regeneration. The transplantation of autologous bone marrow-derived CD34 + cells improved perfusion of the ungraftable ischemic area.

Bone Marrow Cells↗