Loading…
Cell clonality in hypereosinophilic syndrome : what pathogenetic role?
Idiopathic hypereosinophilic syndrome (HES) is a heterogeneous disorder, including either a myeloproliferative or a lymphoproliferative variant (l-HES). In l-HES, T-lymphocytes could be involved in the pathogenesis through several cytokines, including IL5. We assayed both TCR Beta- and delta-rearran...
Saved in:
| Published in: | Clinical and experimental rheumatology 2007, Vol.25 (1), p.17-22 |
|---|---|
| Main Authors: | , , , , , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | |
|---|---|
| cites | |
| container_end_page | 22 |
| container_issue | 1 |
| container_start_page | 17 |
| container_title | Clinical and experimental rheumatology |
| container_volume | 25 |
| creator | GALIMBERTI, S CIABATTI, E OTTIMO, F ROSSI, A TROMBI, L CARULLI, G CERVETTI, G MATTII, L BIANCHI, G PETRINI, M |
| description | Idiopathic hypereosinophilic syndrome (HES) is a heterogeneous disorder, including either a myeloproliferative or a lymphoproliferative variant (l-HES). In l-HES, T-lymphocytes could be involved in the pathogenesis through several cytokines, including IL5.
We assayed both TCR Beta- and delta-rearrangements by fluorescent PCR, characterizing 14 patients affected by HES. Lyn activation (a src-kinase involved in the IL5 pathway) was also tested in 6 cases.
FIP1L1-PDGFRa was detected in 4 cases (28.6%); a clonal TCR was found in 10 cases (71.4%), including cases FIP1L1-PDGFRalpha-positive; four cases did not show any molecular marker. In this series, levels of IL5, IL4, IL2 and gammaIFN were measured, without any significant difference among different subgroups. All pathological samples tested did not show Lyn activation. Immunophenotype was also characterized: only one case showed an atypical CD3-/CD4+ population in the bone marrow.
This study would suggest that a real distinction between m- and l-HES is not wholly convincing and that clonal T-cell expansion could not be the "primum movens" but an epiphenomenon in HES. |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_70356839</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>70356839</sourcerecordid><originalsourceid>FETCH-LOGICAL-p239t-898fd76f60f3984b825d5d6c3865302262bdba75e9f97d564a109203fd6a44843</originalsourceid><addsrcrecordid>eNpFz81KxDAABOAgiruuvoLkordCmjR_XkQWV4UFLwp7K2mT2Eia1KSL9O0tWPE0h_kYmBOwLqkkBZLicArWiEhcCMoOK3CR8ydCmFHGz8Gq5FXJpaBrsNsa72HrY1DejRN0AXbTYJKJ2YU4dM67FuYp6BR7A-_gd6dGOKixix8mmHEuU_Tm_hKcWeWzuVpyA953j2_b52L_-vSyfdgXAyZyLIQUVnNmGbJEiqoRmGqqWUsEowRhzHCjG8WpkVZyTVmlSiQxIlYzVVWiIhtw-7s7pPh1NHmse5fb-YIKJh5zzRGhTBA5w-sFHpve6HpIrldpqv-ez-BmASq3ytukQuvyvxNsloyRH86NYl0</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>70356839</pqid></control><display><type>article</type><title>Cell clonality in hypereosinophilic syndrome : what pathogenetic role?</title><source>Freely Accessible Science Journals - check A-Z of ejournals</source><creator>GALIMBERTI, S ; CIABATTI, E ; OTTIMO, F ; ROSSI, A ; TROMBI, L ; CARULLI, G ; CERVETTI, G ; MATTII, L ; BIANCHI, G ; PETRINI, M</creator><creatorcontrib>GALIMBERTI, S ; CIABATTI, E ; OTTIMO, F ; ROSSI, A ; TROMBI, L ; CARULLI, G ; CERVETTI, G ; MATTII, L ; BIANCHI, G ; PETRINI, M</creatorcontrib><description>Idiopathic hypereosinophilic syndrome (HES) is a heterogeneous disorder, including either a myeloproliferative or a lymphoproliferative variant (l-HES). In l-HES, T-lymphocytes could be involved in the pathogenesis through several cytokines, including IL5.
We assayed both TCR Beta- and delta-rearrangements by fluorescent PCR, characterizing 14 patients affected by HES. Lyn activation (a src-kinase involved in the IL5 pathway) was also tested in 6 cases.
FIP1L1-PDGFRa was detected in 4 cases (28.6%); a clonal TCR was found in 10 cases (71.4%), including cases FIP1L1-PDGFRalpha-positive; four cases did not show any molecular marker. In this series, levels of IL5, IL4, IL2 and gammaIFN were measured, without any significant difference among different subgroups. All pathological samples tested did not show Lyn activation. Immunophenotype was also characterized: only one case showed an atypical CD3-/CD4+ population in the bone marrow.
This study would suggest that a real distinction between m- and l-HES is not wholly convincing and that clonal T-cell expansion could not be the "primum movens" but an epiphenomenon in HES.</description><identifier>ISSN: 0392-856X</identifier><identifier>EISSN: 1593-098X</identifier><identifier>PMID: 17417985</identifier><language>eng</language><publisher>Pisa: Clinical and Experimental Rheumatology</publisher><subject>Adult ; Aged ; Benzamides ; Biological and medical sciences ; Cytokines - analysis ; Cytokines - genetics ; Eosinophils - classification ; Eosinophils - drug effects ; Eosinophils - pathology ; Female ; Hematologic and hematopoietic diseases ; Humans ; Hypereosinophilic Syndrome - genetics ; Hypereosinophilic Syndrome - immunology ; Hypereosinophilic Syndrome - physiopathology ; Imatinib Mesylate ; Immunologic Factors - pharmacology ; Interferon-alpha - pharmacology ; Male ; Medical sciences ; Middle Aged ; mRNA Cleavage and Polyadenylation Factors - blood ; Oncogene Proteins, Fusion - blood ; Other diseases. Hematologic involvement in other diseases ; Piperazines - pharmacology ; Protein Kinase Inhibitors - pharmacology ; Pyrimidines - pharmacology ; Receptor, Platelet-Derived Growth Factor alpha - blood ; Retrospective Studies ; T-Lymphocytes - metabolism</subject><ispartof>Clinical and experimental rheumatology, 2007, Vol.25 (1), p.17-22</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18674166$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17417985$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GALIMBERTI, S</creatorcontrib><creatorcontrib>CIABATTI, E</creatorcontrib><creatorcontrib>OTTIMO, F</creatorcontrib><creatorcontrib>ROSSI, A</creatorcontrib><creatorcontrib>TROMBI, L</creatorcontrib><creatorcontrib>CARULLI, G</creatorcontrib><creatorcontrib>CERVETTI, G</creatorcontrib><creatorcontrib>MATTII, L</creatorcontrib><creatorcontrib>BIANCHI, G</creatorcontrib><creatorcontrib>PETRINI, M</creatorcontrib><title>Cell clonality in hypereosinophilic syndrome : what pathogenetic role?</title><title>Clinical and experimental rheumatology</title><addtitle>Clin Exp Rheumatol</addtitle><description>Idiopathic hypereosinophilic syndrome (HES) is a heterogeneous disorder, including either a myeloproliferative or a lymphoproliferative variant (l-HES). In l-HES, T-lymphocytes could be involved in the pathogenesis through several cytokines, including IL5.
We assayed both TCR Beta- and delta-rearrangements by fluorescent PCR, characterizing 14 patients affected by HES. Lyn activation (a src-kinase involved in the IL5 pathway) was also tested in 6 cases.
FIP1L1-PDGFRa was detected in 4 cases (28.6%); a clonal TCR was found in 10 cases (71.4%), including cases FIP1L1-PDGFRalpha-positive; four cases did not show any molecular marker. In this series, levels of IL5, IL4, IL2 and gammaIFN were measured, without any significant difference among different subgroups. All pathological samples tested did not show Lyn activation. Immunophenotype was also characterized: only one case showed an atypical CD3-/CD4+ population in the bone marrow.
This study would suggest that a real distinction between m- and l-HES is not wholly convincing and that clonal T-cell expansion could not be the "primum movens" but an epiphenomenon in HES.</description><subject>Adult</subject><subject>Aged</subject><subject>Benzamides</subject><subject>Biological and medical sciences</subject><subject>Cytokines - analysis</subject><subject>Cytokines - genetics</subject><subject>Eosinophils - classification</subject><subject>Eosinophils - drug effects</subject><subject>Eosinophils - pathology</subject><subject>Female</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Hypereosinophilic Syndrome - genetics</subject><subject>Hypereosinophilic Syndrome - immunology</subject><subject>Hypereosinophilic Syndrome - physiopathology</subject><subject>Imatinib Mesylate</subject><subject>Immunologic Factors - pharmacology</subject><subject>Interferon-alpha - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>mRNA Cleavage and Polyadenylation Factors - blood</subject><subject>Oncogene Proteins, Fusion - blood</subject><subject>Other diseases. Hematologic involvement in other diseases</subject><subject>Piperazines - pharmacology</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Pyrimidines - pharmacology</subject><subject>Receptor, Platelet-Derived Growth Factor alpha - blood</subject><subject>Retrospective Studies</subject><subject>T-Lymphocytes - metabolism</subject><issn>0392-856X</issn><issn>1593-098X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNpFz81KxDAABOAgiruuvoLkordCmjR_XkQWV4UFLwp7K2mT2Eia1KSL9O0tWPE0h_kYmBOwLqkkBZLicArWiEhcCMoOK3CR8ydCmFHGz8Gq5FXJpaBrsNsa72HrY1DejRN0AXbTYJKJ2YU4dM67FuYp6BR7A-_gd6dGOKixix8mmHEuU_Tm_hKcWeWzuVpyA953j2_b52L_-vSyfdgXAyZyLIQUVnNmGbJEiqoRmGqqWUsEowRhzHCjG8WpkVZyTVmlSiQxIlYzVVWiIhtw-7s7pPh1NHmse5fb-YIKJh5zzRGhTBA5w-sFHpve6HpIrldpqv-ez-BmASq3ytukQuvyvxNsloyRH86NYl0</recordid><startdate>2007</startdate><enddate>2007</enddate><creator>GALIMBERTI, S</creator><creator>CIABATTI, E</creator><creator>OTTIMO, F</creator><creator>ROSSI, A</creator><creator>TROMBI, L</creator><creator>CARULLI, G</creator><creator>CERVETTI, G</creator><creator>MATTII, L</creator><creator>BIANCHI, G</creator><creator>PETRINI, M</creator><general>Clinical and Experimental Rheumatology</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>2007</creationdate><title>Cell clonality in hypereosinophilic syndrome : what pathogenetic role?</title><author>GALIMBERTI, S ; CIABATTI, E ; OTTIMO, F ; ROSSI, A ; TROMBI, L ; CARULLI, G ; CERVETTI, G ; MATTII, L ; BIANCHI, G ; PETRINI, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p239t-898fd76f60f3984b825d5d6c3865302262bdba75e9f97d564a109203fd6a44843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Benzamides</topic><topic>Biological and medical sciences</topic><topic>Cytokines - analysis</topic><topic>Cytokines - genetics</topic><topic>Eosinophils - classification</topic><topic>Eosinophils - drug effects</topic><topic>Eosinophils - pathology</topic><topic>Female</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Hypereosinophilic Syndrome - genetics</topic><topic>Hypereosinophilic Syndrome - immunology</topic><topic>Hypereosinophilic Syndrome - physiopathology</topic><topic>Imatinib Mesylate</topic><topic>Immunologic Factors - pharmacology</topic><topic>Interferon-alpha - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>mRNA Cleavage and Polyadenylation Factors - blood</topic><topic>Oncogene Proteins, Fusion - blood</topic><topic>Other diseases. Hematologic involvement in other diseases</topic><topic>Piperazines - pharmacology</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Pyrimidines - pharmacology</topic><topic>Receptor, Platelet-Derived Growth Factor alpha - blood</topic><topic>Retrospective Studies</topic><topic>T-Lymphocytes - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GALIMBERTI, S</creatorcontrib><creatorcontrib>CIABATTI, E</creatorcontrib><creatorcontrib>OTTIMO, F</creatorcontrib><creatorcontrib>ROSSI, A</creatorcontrib><creatorcontrib>TROMBI, L</creatorcontrib><creatorcontrib>CARULLI, G</creatorcontrib><creatorcontrib>CERVETTI, G</creatorcontrib><creatorcontrib>MATTII, L</creatorcontrib><creatorcontrib>BIANCHI, G</creatorcontrib><creatorcontrib>PETRINI, M</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental rheumatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GALIMBERTI, S</au><au>CIABATTI, E</au><au>OTTIMO, F</au><au>ROSSI, A</au><au>TROMBI, L</au><au>CARULLI, G</au><au>CERVETTI, G</au><au>MATTII, L</au><au>BIANCHI, G</au><au>PETRINI, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cell clonality in hypereosinophilic syndrome : what pathogenetic role?</atitle><jtitle>Clinical and experimental rheumatology</jtitle><addtitle>Clin Exp Rheumatol</addtitle><date>2007</date><risdate>2007</risdate><volume>25</volume><issue>1</issue><spage>17</spage><epage>22</epage><pages>17-22</pages><issn>0392-856X</issn><eissn>1593-098X</eissn><abstract>Idiopathic hypereosinophilic syndrome (HES) is a heterogeneous disorder, including either a myeloproliferative or a lymphoproliferative variant (l-HES). In l-HES, T-lymphocytes could be involved in the pathogenesis through several cytokines, including IL5.
We assayed both TCR Beta- and delta-rearrangements by fluorescent PCR, characterizing 14 patients affected by HES. Lyn activation (a src-kinase involved in the IL5 pathway) was also tested in 6 cases.
FIP1L1-PDGFRa was detected in 4 cases (28.6%); a clonal TCR was found in 10 cases (71.4%), including cases FIP1L1-PDGFRalpha-positive; four cases did not show any molecular marker. In this series, levels of IL5, IL4, IL2 and gammaIFN were measured, without any significant difference among different subgroups. All pathological samples tested did not show Lyn activation. Immunophenotype was also characterized: only one case showed an atypical CD3-/CD4+ population in the bone marrow.
This study would suggest that a real distinction between m- and l-HES is not wholly convincing and that clonal T-cell expansion could not be the "primum movens" but an epiphenomenon in HES.</abstract><cop>Pisa</cop><pub>Clinical and Experimental Rheumatology</pub><pmid>17417985</pmid><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0392-856X |
| ispartof | Clinical and experimental rheumatology, 2007, Vol.25 (1), p.17-22 |
| issn | 0392-856X 1593-098X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_70356839 |
| source | Freely Accessible Science Journals - check A-Z of ejournals |
| subjects | Adult Aged Benzamides Biological and medical sciences Cytokines - analysis Cytokines - genetics Eosinophils - classification Eosinophils - drug effects Eosinophils - pathology Female Hematologic and hematopoietic diseases Humans Hypereosinophilic Syndrome - genetics Hypereosinophilic Syndrome - immunology Hypereosinophilic Syndrome - physiopathology Imatinib Mesylate Immunologic Factors - pharmacology Interferon-alpha - pharmacology Male Medical sciences Middle Aged mRNA Cleavage and Polyadenylation Factors - blood Oncogene Proteins, Fusion - blood Other diseases. Hematologic involvement in other diseases Piperazines - pharmacology Protein Kinase Inhibitors - pharmacology Pyrimidines - pharmacology Receptor, Platelet-Derived Growth Factor alpha - blood Retrospective Studies T-Lymphocytes - metabolism |
| title | Cell clonality in hypereosinophilic syndrome : what pathogenetic role? |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-04T17%3A48%3A45IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cell%20clonality%20in%20hypereosinophilic%20syndrome%20:%20what%20pathogenetic%20role?&rft.jtitle=Clinical%20and%20experimental%20rheumatology&rft.au=GALIMBERTI,%20S&rft.date=2007&rft.volume=25&rft.issue=1&rft.spage=17&rft.epage=22&rft.pages=17-22&rft.issn=0392-856X&rft.eissn=1593-098X&rft_id=info:doi/&rft_dat=%3Cproquest_pubme%3E70356839%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-p239t-898fd76f60f3984b825d5d6c3865302262bdba75e9f97d564a109203fd6a44843%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=70356839&rft_id=info:pmid/17417985&rfr_iscdi=true |