Detailed immunophenotypic characterization of different major and minor subsets of peripheral blood cells in patients with paroxysmal nocturnal hemoglobinuria
BACKGROUND: Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by a deficient expression of glycosylphosphatidylinositol‐anchored proteins (GPI‐APs), due to somatic mutations of the phosphatidylinositolglycan complementation Class A (PIG‐A) gene. STUDY DESIGN AND METHODS: In this study, the...
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| Veröffentlicht in: | Transfusion (Philadelphia, Pa.) Pa.), 2008-07, Vol.48 (7), p.1403-1414 |
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| creator | Hernández-Campo, Pilar M. Almeida, Julia Acevedo, María J. Sánchez, María L. Alberca, Ignacio Vidriales, Belén Martínez, Elvira Romero, Juan R. Orfao, Alberto |
| description | BACKGROUND: Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by a deficient expression of glycosylphosphatidylinositol‐anchored proteins (GPI‐APs), due to somatic mutations of the phosphatidylinositolglycan complementation Class A (PIG‐A) gene.
STUDY DESIGN AND METHODS: In this study, the expression of a high number of GPI‐APs on different subsets of peripheral blood (PB) cells from 14 PNH patients and their potential association with underlying genetic abnormalities has been analyzed.
RESULTS: This study confirms the existence of variable patterns of expression of different GPI‐APs on both major and minor PB‐cell subsets from PNH patients. The size of the PNH clone within PB neutrophils and monocytes was systematically higher than that of other cell populations. Genetic changes were detected in the PIG‐A gene in 5 of 13 cases analyzed. Interestingly, the reactivity for many GPI‐APs was significantly higher on different subsets of normal PB cells from PNH patients than those observed on healthy volunteers.
CONCLUSION: The best combination of markers for the diagnostic screening of PNH would include evaluation of CD14 on monocytes and of CD16 on neutrophils, although further analysis of CD55 and CD59 expression may contain additional clinically useful information. Clear association between the genetic changes detected in the PIG‐A gene in 5 of 13 cases analyzed, and the phenotypic profile of PNH cells has not been found. Additionally, an abnormally higher expression of several GPI‐APs among normal residual cells from PNH patients in comparison to healthy donors was observed, suggesting that factors other than the PIG‐A mutation could determine the phenotypic profile of PB cells in PNH. |
| doi_str_mv | 10.1111/j.1537-2995.2008.01686.x |
| format | Article |
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STUDY DESIGN AND METHODS: In this study, the expression of a high number of GPI‐APs on different subsets of peripheral blood (PB) cells from 14 PNH patients and their potential association with underlying genetic abnormalities has been analyzed.
RESULTS: This study confirms the existence of variable patterns of expression of different GPI‐APs on both major and minor PB‐cell subsets from PNH patients. The size of the PNH clone within PB neutrophils and monocytes was systematically higher than that of other cell populations. Genetic changes were detected in the PIG‐A gene in 5 of 13 cases analyzed. Interestingly, the reactivity for many GPI‐APs was significantly higher on different subsets of normal PB cells from PNH patients than those observed on healthy volunteers.
CONCLUSION: The best combination of markers for the diagnostic screening of PNH would include evaluation of CD14 on monocytes and of CD16 on neutrophils, although further analysis of CD55 and CD59 expression may contain additional clinically useful information. Clear association between the genetic changes detected in the PIG‐A gene in 5 of 13 cases analyzed, and the phenotypic profile of PNH cells has not been found. Additionally, an abnormally higher expression of several GPI‐APs among normal residual cells from PNH patients in comparison to healthy donors was observed, suggesting that factors other than the PIG‐A mutation could determine the phenotypic profile of PB cells in PNH.</description><identifier>ISSN: 0041-1132</identifier><identifier>EISSN: 1537-2995</identifier><identifier>DOI: 10.1111/j.1537-2995.2008.01686.x</identifier><identifier>PMID: 18422849</identifier><identifier>CODEN: TRANAT</identifier><language>eng</language><publisher>Malden, USA: Blackwell Publishing Inc</publisher><subject>ADP-ribosyl Cyclase - blood ; Adult ; Aged ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Antigens, CD - blood ; Biological and medical sciences ; Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis ; Bone marrow, stem cells transplantation. Graft versus host reaction ; CD24 Antigen - blood ; CD55 Antigens - blood ; CD59 Antigens - blood ; Female ; GPI-Linked Proteins ; Hemoglobinuria, Paroxysmal - blood ; Hemoglobinuria, Paroxysmal - genetics ; Hemoglobinuria, Paroxysmal - immunology ; Humans ; Immunophenotyping - methods ; Lipopolysaccharide Receptors - blood ; Male ; Medical sciences ; Membrane Cofactor Protein - blood ; Membrane Proteins - blood ; Membrane Proteins - genetics ; Middle Aged ; Monocytes - cytology ; Monocytes - immunology ; Monocytes - metabolism ; Mutation ; Neutrophils - cytology ; Neutrophils - immunology ; Neutrophils - metabolism ; Receptors, IgG - blood ; Transfusions. Complications. Transfusion reactions. Cell and gene therapy</subject><ispartof>Transfusion (Philadelphia, Pa.), 2008-07, Vol.48 (7), p.1403-1414</ispartof><rights>2008 American Association of Blood Banks</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4366-d4264e94c8399a51ff1260ac9a9884e6a415a6ca737bd08db1e4359b2efb84c93</citedby><cites>FETCH-LOGICAL-c4366-d4264e94c8399a51ff1260ac9a9884e6a415a6ca737bd08db1e4359b2efb84c93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1537-2995.2008.01686.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1537-2995.2008.01686.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20498398$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18422849$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hernández-Campo, Pilar M.</creatorcontrib><creatorcontrib>Almeida, Julia</creatorcontrib><creatorcontrib>Acevedo, María J.</creatorcontrib><creatorcontrib>Sánchez, María L.</creatorcontrib><creatorcontrib>Alberca, Ignacio</creatorcontrib><creatorcontrib>Vidriales, Belén</creatorcontrib><creatorcontrib>Martínez, Elvira</creatorcontrib><creatorcontrib>Romero, Juan R.</creatorcontrib><creatorcontrib>Orfao, Alberto</creatorcontrib><title>Detailed immunophenotypic characterization of different major and minor subsets of peripheral blood cells in patients with paroxysmal nocturnal hemoglobinuria</title><title>Transfusion (Philadelphia, Pa.)</title><addtitle>Transfusion</addtitle><description>BACKGROUND: Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by a deficient expression of glycosylphosphatidylinositol‐anchored proteins (GPI‐APs), due to somatic mutations of the phosphatidylinositolglycan complementation Class A (PIG‐A) gene.
STUDY DESIGN AND METHODS: In this study, the expression of a high number of GPI‐APs on different subsets of peripheral blood (PB) cells from 14 PNH patients and their potential association with underlying genetic abnormalities has been analyzed.
RESULTS: This study confirms the existence of variable patterns of expression of different GPI‐APs on both major and minor PB‐cell subsets from PNH patients. The size of the PNH clone within PB neutrophils and monocytes was systematically higher than that of other cell populations. Genetic changes were detected in the PIG‐A gene in 5 of 13 cases analyzed. Interestingly, the reactivity for many GPI‐APs was significantly higher on different subsets of normal PB cells from PNH patients than those observed on healthy volunteers.
CONCLUSION: The best combination of markers for the diagnostic screening of PNH would include evaluation of CD14 on monocytes and of CD16 on neutrophils, although further analysis of CD55 and CD59 expression may contain additional clinically useful information. Clear association between the genetic changes detected in the PIG‐A gene in 5 of 13 cases analyzed, and the phenotypic profile of PNH cells has not been found. Additionally, an abnormally higher expression of several GPI‐APs among normal residual cells from PNH patients in comparison to healthy donors was observed, suggesting that factors other than the PIG‐A mutation could determine the phenotypic profile of PB cells in PNH.</description><subject>ADP-ribosyl Cyclase - blood</subject><subject>Adult</subject><subject>Aged</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Antigens, CD - blood</subject><subject>Biological and medical sciences</subject><subject>Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis</subject><subject>Bone marrow, stem cells transplantation. Graft versus host reaction</subject><subject>CD24 Antigen - blood</subject><subject>CD55 Antigens - blood</subject><subject>CD59 Antigens - blood</subject><subject>Female</subject><subject>GPI-Linked Proteins</subject><subject>Hemoglobinuria, Paroxysmal - blood</subject><subject>Hemoglobinuria, Paroxysmal - genetics</subject><subject>Hemoglobinuria, Paroxysmal - immunology</subject><subject>Humans</subject><subject>Immunophenotyping - methods</subject><subject>Lipopolysaccharide Receptors - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Cofactor Protein - blood</subject><subject>Membrane Proteins - blood</subject><subject>Membrane Proteins - genetics</subject><subject>Middle Aged</subject><subject>Monocytes - cytology</subject><subject>Monocytes - immunology</subject><subject>Monocytes - metabolism</subject><subject>Mutation</subject><subject>Neutrophils - cytology</subject><subject>Neutrophils - immunology</subject><subject>Neutrophils - metabolism</subject><subject>Receptors, IgG - blood</subject><subject>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</subject><issn>0041-1132</issn><issn>1537-2995</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkdGOEyEUhonRuHX1FQw3ejcVGIbCjYlZbdVsNDFVL8kZhrHUGRhhJtv6MD6rzLapt3LDIXz_fw78CGFKljSvV_slrcpVwZSqlowQuSRUSLE8PECLy8VDtCCE04LSkl2hJyntCSFMEfoYXVHJGZNcLdCft3YE19kGu76ffBh21ofxODiDzQ4imNFG9xtGFzwOLW5c29po_Yh72IeIwTe4dz5XaaqTHdMMDVmSfSJ0uO5CaLCxXZew83jIRlmc8J0bd_kUw-GY-sz5YMYp-lztbB9-dKF2fooOnqJHLXTJPjvv1-jr-t325n1x-3nz4ebNbWF4KUTRcCa4VdzIUimoaNtSJggYBUpKbgVwWoEwsCpXdUNkU1PLy0rVzLa15EaV1-jlyXeI4ddk06h7l-axwdswJS1UyUWlqgzKE2hiSCnaVg_R9RCPmhI9Z6P3eo5AzxHoORt9n40-ZOnzc4-p7m3zT3gOIwMvzgAkA10bwRuXLhwjXOX3ycy9PnF3Objjfw-gt1_W92U2KE4GLo32cDGA-FOL_EWV_v5po9X6W1VtNx_1pvwLSLi-4g</recordid><startdate>200807</startdate><enddate>200807</enddate><creator>Hernández-Campo, Pilar M.</creator><creator>Almeida, Julia</creator><creator>Acevedo, María J.</creator><creator>Sánchez, María L.</creator><creator>Alberca, Ignacio</creator><creator>Vidriales, Belén</creator><creator>Martínez, Elvira</creator><creator>Romero, Juan R.</creator><creator>Orfao, Alberto</creator><general>Blackwell Publishing Inc</general><general>Blackwell Publishing</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200807</creationdate><title>Detailed immunophenotypic characterization of different major and minor subsets of peripheral blood cells in patients with paroxysmal nocturnal hemoglobinuria</title><author>Hernández-Campo, Pilar M. ; Almeida, Julia ; Acevedo, María J. ; Sánchez, María L. ; Alberca, Ignacio ; Vidriales, Belén ; Martínez, Elvira ; Romero, Juan R. ; Orfao, Alberto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4366-d4264e94c8399a51ff1260ac9a9884e6a415a6ca737bd08db1e4359b2efb84c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>ADP-ribosyl Cyclase - blood</topic><topic>Adult</topic><topic>Aged</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Antigens, CD - blood</topic><topic>Biological and medical sciences</topic><topic>Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis</topic><topic>Bone marrow, stem cells transplantation. Graft versus host reaction</topic><topic>CD24 Antigen - blood</topic><topic>CD55 Antigens - blood</topic><topic>CD59 Antigens - blood</topic><topic>Female</topic><topic>GPI-Linked Proteins</topic><topic>Hemoglobinuria, Paroxysmal - blood</topic><topic>Hemoglobinuria, Paroxysmal - genetics</topic><topic>Hemoglobinuria, Paroxysmal - immunology</topic><topic>Humans</topic><topic>Immunophenotyping - methods</topic><topic>Lipopolysaccharide Receptors - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Cofactor Protein - blood</topic><topic>Membrane Proteins - blood</topic><topic>Membrane Proteins - genetics</topic><topic>Middle Aged</topic><topic>Monocytes - cytology</topic><topic>Monocytes - immunology</topic><topic>Monocytes - metabolism</topic><topic>Mutation</topic><topic>Neutrophils - cytology</topic><topic>Neutrophils - immunology</topic><topic>Neutrophils - metabolism</topic><topic>Receptors, IgG - blood</topic><topic>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hernández-Campo, Pilar M.</creatorcontrib><creatorcontrib>Almeida, Julia</creatorcontrib><creatorcontrib>Acevedo, María J.</creatorcontrib><creatorcontrib>Sánchez, María L.</creatorcontrib><creatorcontrib>Alberca, Ignacio</creatorcontrib><creatorcontrib>Vidriales, Belén</creatorcontrib><creatorcontrib>Martínez, Elvira</creatorcontrib><creatorcontrib>Romero, Juan R.</creatorcontrib><creatorcontrib>Orfao, Alberto</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Transfusion (Philadelphia, Pa.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hernández-Campo, Pilar M.</au><au>Almeida, Julia</au><au>Acevedo, María J.</au><au>Sánchez, María L.</au><au>Alberca, Ignacio</au><au>Vidriales, Belén</au><au>Martínez, Elvira</au><au>Romero, Juan R.</au><au>Orfao, Alberto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Detailed immunophenotypic characterization of different major and minor subsets of peripheral blood cells in patients with paroxysmal nocturnal hemoglobinuria</atitle><jtitle>Transfusion (Philadelphia, Pa.)</jtitle><addtitle>Transfusion</addtitle><date>2008-07</date><risdate>2008</risdate><volume>48</volume><issue>7</issue><spage>1403</spage><epage>1414</epage><pages>1403-1414</pages><issn>0041-1132</issn><eissn>1537-2995</eissn><coden>TRANAT</coden><abstract>BACKGROUND: Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by a deficient expression of glycosylphosphatidylinositol‐anchored proteins (GPI‐APs), due to somatic mutations of the phosphatidylinositolglycan complementation Class A (PIG‐A) gene.
STUDY DESIGN AND METHODS: In this study, the expression of a high number of GPI‐APs on different subsets of peripheral blood (PB) cells from 14 PNH patients and their potential association with underlying genetic abnormalities has been analyzed.
RESULTS: This study confirms the existence of variable patterns of expression of different GPI‐APs on both major and minor PB‐cell subsets from PNH patients. The size of the PNH clone within PB neutrophils and monocytes was systematically higher than that of other cell populations. Genetic changes were detected in the PIG‐A gene in 5 of 13 cases analyzed. Interestingly, the reactivity for many GPI‐APs was significantly higher on different subsets of normal PB cells from PNH patients than those observed on healthy volunteers.
CONCLUSION: The best combination of markers for the diagnostic screening of PNH would include evaluation of CD14 on monocytes and of CD16 on neutrophils, although further analysis of CD55 and CD59 expression may contain additional clinically useful information. Clear association between the genetic changes detected in the PIG‐A gene in 5 of 13 cases analyzed, and the phenotypic profile of PNH cells has not been found. Additionally, an abnormally higher expression of several GPI‐APs among normal residual cells from PNH patients in comparison to healthy donors was observed, suggesting that factors other than the PIG‐A mutation could determine the phenotypic profile of PB cells in PNH.</abstract><cop>Malden, USA</cop><pub>Blackwell Publishing Inc</pub><pmid>18422849</pmid><doi>10.1111/j.1537-2995.2008.01686.x</doi><tpages>12</tpages></addata></record> |
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| subjects | ADP-ribosyl Cyclase - blood Adult Aged Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Antigens, CD - blood Biological and medical sciences Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis Bone marrow, stem cells transplantation. Graft versus host reaction CD24 Antigen - blood CD55 Antigens - blood CD59 Antigens - blood Female GPI-Linked Proteins Hemoglobinuria, Paroxysmal - blood Hemoglobinuria, Paroxysmal - genetics Hemoglobinuria, Paroxysmal - immunology Humans Immunophenotyping - methods Lipopolysaccharide Receptors - blood Male Medical sciences Membrane Cofactor Protein - blood Membrane Proteins - blood Membrane Proteins - genetics Middle Aged Monocytes - cytology Monocytes - immunology Monocytes - metabolism Mutation Neutrophils - cytology Neutrophils - immunology Neutrophils - metabolism Receptors, IgG - blood Transfusions. Complications. Transfusion reactions. Cell and gene therapy |
| title | Detailed immunophenotypic characterization of different major and minor subsets of peripheral blood cells in patients with paroxysmal nocturnal hemoglobinuria |
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