Fcγ receptor expression on splenic macrophages in adult immune thrombocytopenia
Summary Splenic macrophages play a key role in immune thrombocytopenia (ITP) pathogenesis by clearing opsonized platelets. Fcγ receptors (FcγR) participate in this phenomenon, but their expression on splenic macrophages and their modulation by treatment have scarcely been studied in human ITP. We ai...
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| Veröffentlicht in: | Clinical and experimental immunology 2017-05, Vol.188 (2), p.275-282 |
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| creator | Audia, S. Santegoets, K. Laarhoven, A. G. Vidarsson, G. Facy, O. Ortega‐Deballon, P. Samson, M. Janikashvili, N. Saas, P. Bonnotte, B. Radstake, T. R. |
| description | Summary
Splenic macrophages play a key role in immune thrombocytopenia (ITP) pathogenesis by clearing opsonized platelets. Fcγ receptors (FcγR) participate in this phenomenon, but their expression on splenic macrophages and their modulation by treatment have scarcely been studied in human ITP. We aimed to compare the phenotype and function of splenic macrophages between six controls and 24 ITP patients and between ITP patients according to the treatments they received prior to splenectomy. CD86, human leucocyte antigen D‐related (HLA‐DR) and FcγR expression were measured by flow cytometry on splenic macrophages. The major FcγR polymorphisms were determined and splenic macrophage function was assessed by a phagocytosis assay. The expression of the activation markers CD86 and HLA‐DR was higher on splenic macrophages during ITP compared to controls. While the expression of FcγR was not different between ITP and controls, the phagocytic function of splenic macrophages was reduced in ITP patients treated with intravenous immunoglobulin (IVIg) within the 2 weeks prior to splenectomy. The FCGR3A (158V/F) polymorphism, known to increase the affinity of FcγRIII to IgG, was over‐represented in ITP patients. Thus, these are the first results arguing for the fact that the therapeutic use of IVIg during human chronic ITP does not modulate FcγR expression on splenic macrophages but decreases their phagocytic capabilities.
The expression of activator and inhibitory Fcgamma receptors on splenic macrophages is not imbalance during immune thrombocytopenia. Most particularly, IVIg given within the two weeks prior to splenectomy do not increase the expression of the inhibitory receptor FcgammaRIIb. |
| doi_str_mv | 10.1111/cei.12935 |
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Splenic macrophages play a key role in immune thrombocytopenia (ITP) pathogenesis by clearing opsonized platelets. Fcγ receptors (FcγR) participate in this phenomenon, but their expression on splenic macrophages and their modulation by treatment have scarcely been studied in human ITP. We aimed to compare the phenotype and function of splenic macrophages between six controls and 24 ITP patients and between ITP patients according to the treatments they received prior to splenectomy. CD86, human leucocyte antigen D‐related (HLA‐DR) and FcγR expression were measured by flow cytometry on splenic macrophages. The major FcγR polymorphisms were determined and splenic macrophage function was assessed by a phagocytosis assay. The expression of the activation markers CD86 and HLA‐DR was higher on splenic macrophages during ITP compared to controls. While the expression of FcγR was not different between ITP and controls, the phagocytic function of splenic macrophages was reduced in ITP patients treated with intravenous immunoglobulin (IVIg) within the 2 weeks prior to splenectomy. The FCGR3A (158V/F) polymorphism, known to increase the affinity of FcγRIII to IgG, was over‐represented in ITP patients. Thus, these are the first results arguing for the fact that the therapeutic use of IVIg during human chronic ITP does not modulate FcγR expression on splenic macrophages but decreases their phagocytic capabilities.
The expression of activator and inhibitory Fcgamma receptors on splenic macrophages is not imbalance during immune thrombocytopenia. Most particularly, IVIg given within the two weeks prior to splenectomy do not increase the expression of the inhibitory receptor FcgammaRIIb.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/cei.12935</identifier><identifier>PMID: 28142207</identifier><language>eng</language><publisher>England: Wiley</publisher><subject>Adult ; Aged ; Antigens, CD86 ; Autoimmune Diseases ; Autoimmune Diseases - immunology ; Autoimmune Diseases - surgery ; Autoimmune Diseases - therapy ; autoimmunity ; B7-2 Antigen - analysis ; Fc receptors ; Female ; Flow Cytometry ; Humans ; Immunoglobulin G ; Immunoglobulin G - blood ; Immunoglobulins, Intravenous ; Immunoglobulins, Intravenous - therapeutic use ; Immunology ; Life Sciences ; Macrophages ; Macrophages - immunology ; Macrophages - physiology ; Male ; Middle Aged ; Original ; Phagocytosis ; Phenotype ; Polymorphism, Genetic ; Receptors, IgG ; Receptors, IgG - analysis ; Receptors, IgG - genetics ; Receptors, IgG - immunology ; Spleen ; Spleen - cytology ; Spleen - immunology ; Splenectomy ; Thrombocytopenia ; Thrombocytopenia - immunology ; Thrombocytopenia - surgery ; Thrombocytopenia - therapy</subject><ispartof>Clinical and experimental immunology, 2017-05, Vol.188 (2), p.275-282</ispartof><rights>2017 British Society for Immunology</rights><rights>2017 British Society for Immunology.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4825-205213d660cf369e02cf127890560c05e50da56b71907ba937df3eb75b694f0e3</citedby><cites>FETCH-LOGICAL-c4825-205213d660cf369e02cf127890560c05e50da56b71907ba937df3eb75b694f0e3</cites><orcidid>0000-0003-1772-1392 ; 0000-0001-7229-3808 ; 0000-0002-1098-4598</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5383444/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5383444/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28142207$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://u-bourgogne.hal.science/hal-01556448$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Audia, S.</creatorcontrib><creatorcontrib>Santegoets, K.</creatorcontrib><creatorcontrib>Laarhoven, A. G.</creatorcontrib><creatorcontrib>Vidarsson, G.</creatorcontrib><creatorcontrib>Facy, O.</creatorcontrib><creatorcontrib>Ortega‐Deballon, P.</creatorcontrib><creatorcontrib>Samson, M.</creatorcontrib><creatorcontrib>Janikashvili, N.</creatorcontrib><creatorcontrib>Saas, P.</creatorcontrib><creatorcontrib>Bonnotte, B.</creatorcontrib><creatorcontrib>Radstake, T. R.</creatorcontrib><title>Fcγ receptor expression on splenic macrophages in adult immune thrombocytopenia</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>Summary
Splenic macrophages play a key role in immune thrombocytopenia (ITP) pathogenesis by clearing opsonized platelets. Fcγ receptors (FcγR) participate in this phenomenon, but their expression on splenic macrophages and their modulation by treatment have scarcely been studied in human ITP. We aimed to compare the phenotype and function of splenic macrophages between six controls and 24 ITP patients and between ITP patients according to the treatments they received prior to splenectomy. CD86, human leucocyte antigen D‐related (HLA‐DR) and FcγR expression were measured by flow cytometry on splenic macrophages. The major FcγR polymorphisms were determined and splenic macrophage function was assessed by a phagocytosis assay. The expression of the activation markers CD86 and HLA‐DR was higher on splenic macrophages during ITP compared to controls. While the expression of FcγR was not different between ITP and controls, the phagocytic function of splenic macrophages was reduced in ITP patients treated with intravenous immunoglobulin (IVIg) within the 2 weeks prior to splenectomy. The FCGR3A (158V/F) polymorphism, known to increase the affinity of FcγRIII to IgG, was over‐represented in ITP patients. Thus, these are the first results arguing for the fact that the therapeutic use of IVIg during human chronic ITP does not modulate FcγR expression on splenic macrophages but decreases their phagocytic capabilities.
The expression of activator and inhibitory Fcgamma receptors on splenic macrophages is not imbalance during immune thrombocytopenia. Most particularly, IVIg given within the two weeks prior to splenectomy do not increase the expression of the inhibitory receptor FcgammaRIIb.</description><subject>Adult</subject><subject>Aged</subject><subject>Antigens, CD86</subject><subject>Autoimmune Diseases</subject><subject>Autoimmune Diseases - immunology</subject><subject>Autoimmune Diseases - surgery</subject><subject>Autoimmune Diseases - therapy</subject><subject>autoimmunity</subject><subject>B7-2 Antigen - analysis</subject><subject>Fc receptors</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Immunoglobulin G</subject><subject>Immunoglobulin G - blood</subject><subject>Immunoglobulins, Intravenous</subject><subject>Immunoglobulins, Intravenous - therapeutic use</subject><subject>Immunology</subject><subject>Life Sciences</subject><subject>Macrophages</subject><subject>Macrophages - immunology</subject><subject>Macrophages - physiology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Original</subject><subject>Phagocytosis</subject><subject>Phenotype</subject><subject>Polymorphism, Genetic</subject><subject>Receptors, IgG</subject><subject>Receptors, IgG - analysis</subject><subject>Receptors, IgG - genetics</subject><subject>Receptors, IgG - immunology</subject><subject>Spleen</subject><subject>Spleen - cytology</subject><subject>Spleen - immunology</subject><subject>Splenectomy</subject><subject>Thrombocytopenia</subject><subject>Thrombocytopenia - immunology</subject><subject>Thrombocytopenia - surgery</subject><subject>Thrombocytopenia - therapy</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS1ERYfCghdAWcJi2uvfxJtK1aillUYqC1hbjnPTMUri1E4K81y8B8-Ey5S2VKqEZcny9XePj30IeUfhkOZx5NAfUqa5fEEWlCu5ZEzol2QBAHqpKYh98jqlb3mrlGKvyD6rqGAMygX5fOZ-_SwiOhynEAv8MUZMyYehyDONHQ7eFb11MYwbe4Wp8ENhm7mbCt_384DFtImhr4PbTmHMsH1D9lrbJXx7tx6Qr2enX1bny_Xlp4vVyXrpRMWyQ5CM8kYpcC1XGoG5lrKy0iBzCSRKaKxUdUk1lLXVvGxajnUpa6VFC8gPyPFOd5zrHhuHwxRtZ8boexu3Jlhv_j0Z_MZchRsjecWFEFng405g86Tt_GRtbmtApVRCVDc0sx_uLovhesY0md4nh11nBwxzMrTStFJUVPI_UMVLkFTCg4P8uylFbO9tUDC3wZocrPkTbGbfP37uPfk3yQwc7YDvvsPt80pmdXqxk_wNuqmtGQ</recordid><startdate>201705</startdate><enddate>201705</enddate><creator>Audia, S.</creator><creator>Santegoets, K.</creator><creator>Laarhoven, A. 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G. ; Vidarsson, G. ; Facy, O. ; Ortega‐Deballon, P. ; Samson, M. ; Janikashvili, N. ; Saas, P. ; Bonnotte, B. ; Radstake, T. 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R.</creatorcontrib><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><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Audia, S.</au><au>Santegoets, K.</au><au>Laarhoven, A. G.</au><au>Vidarsson, G.</au><au>Facy, O.</au><au>Ortega‐Deballon, P.</au><au>Samson, M.</au><au>Janikashvili, N.</au><au>Saas, P.</au><au>Bonnotte, B.</au><au>Radstake, T. R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fcγ receptor expression on splenic macrophages in adult immune thrombocytopenia</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2017-05</date><risdate>2017</risdate><volume>188</volume><issue>2</issue><spage>275</spage><epage>282</epage><pages>275-282</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><abstract>Summary
Splenic macrophages play a key role in immune thrombocytopenia (ITP) pathogenesis by clearing opsonized platelets. Fcγ receptors (FcγR) participate in this phenomenon, but their expression on splenic macrophages and their modulation by treatment have scarcely been studied in human ITP. We aimed to compare the phenotype and function of splenic macrophages between six controls and 24 ITP patients and between ITP patients according to the treatments they received prior to splenectomy. CD86, human leucocyte antigen D‐related (HLA‐DR) and FcγR expression were measured by flow cytometry on splenic macrophages. The major FcγR polymorphisms were determined and splenic macrophage function was assessed by a phagocytosis assay. The expression of the activation markers CD86 and HLA‐DR was higher on splenic macrophages during ITP compared to controls. While the expression of FcγR was not different between ITP and controls, the phagocytic function of splenic macrophages was reduced in ITP patients treated with intravenous immunoglobulin (IVIg) within the 2 weeks prior to splenectomy. The FCGR3A (158V/F) polymorphism, known to increase the affinity of FcγRIII to IgG, was over‐represented in ITP patients. Thus, these are the first results arguing for the fact that the therapeutic use of IVIg during human chronic ITP does not modulate FcγR expression on splenic macrophages but decreases their phagocytic capabilities.
The expression of activator and inhibitory Fcgamma receptors on splenic macrophages is not imbalance during immune thrombocytopenia. Most particularly, IVIg given within the two weeks prior to splenectomy do not increase the expression of the inhibitory receptor FcgammaRIIb.</abstract><cop>England</cop><pub>Wiley</pub><pmid>28142207</pmid><doi>10.1111/cei.12935</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-1772-1392</orcidid><orcidid>https://orcid.org/0000-0001-7229-3808</orcidid><orcidid>https://orcid.org/0000-0002-1098-4598</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Antigens, CD86 Autoimmune Diseases Autoimmune Diseases - immunology Autoimmune Diseases - surgery Autoimmune Diseases - therapy autoimmunity B7-2 Antigen - analysis Fc receptors Female Flow Cytometry Humans Immunoglobulin G Immunoglobulin G - blood Immunoglobulins, Intravenous Immunoglobulins, Intravenous - therapeutic use Immunology Life Sciences Macrophages Macrophages - immunology Macrophages - physiology Male Middle Aged Original Phagocytosis Phenotype Polymorphism, Genetic Receptors, IgG Receptors, IgG - analysis Receptors, IgG - genetics Receptors, IgG - immunology Spleen Spleen - cytology Spleen - immunology Splenectomy Thrombocytopenia Thrombocytopenia - immunology Thrombocytopenia - surgery Thrombocytopenia - therapy |
| title | Fcγ receptor expression on splenic macrophages in adult immune thrombocytopenia |
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