Defects of immunoregulatory mechanisms in myasthenia gravis: role of IL-17
Deficient immunoregulation is consistently observed in autoimmune diseases. Here, we summarize the abnormalities of the T cell response in autoimmune myasthenia gravis (MG) by focusing on activation markers, inflammatory features, and imbalance between the different T cell subsets, including Th17 an...
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| Veröffentlicht in: | Annals of the New York Academy of Sciences 2012-12, Vol.1274 (1), p.40-47 |
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| creator | Gradolatto, Angeline Nazzal, Dani Foti, Maria Bismuth, Jacky Truffault, Frederique Panse, Rozen Le Berrih-Aknin, Sonia |
| description | Deficient immunoregulation is consistently observed in autoimmune diseases. Here, we summarize the abnormalities of the T cell response in autoimmune myasthenia gravis (MG) by focusing on activation markers, inflammatory features, and imbalance between the different T cell subsets, including Th17 and regulatory T cells (Treg cells). In the thymus from MG patients, Treg cell numbers are normal while their suppressive function is severely defective, and this defect could not be explained by contaminating effector CD127low T cells. A transcriptomic analysis of Treg cell and conventional T cell (Tconv; CD4+CD25− cells) subsets pointed out an upregulation of Th17‐related genes in MG cells. Together with our previous findings of an inflammatory signature in the MG thymus and an overproduction of IL‐1 and IL‐6 by MG thymic epithelial cells (TEC), these data strongly suggest that T cell functions are profoundly altered in the thymic pathological environment. In this short review we discuss the mechanisms of chronic inflammation linked to the pathophysiology of MG disease. |
| doi_str_mv | 10.1111/j.1749-6632.2012.06791.x |
| format | Article |
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Here, we summarize the abnormalities of the T cell response in autoimmune myasthenia gravis (MG) by focusing on activation markers, inflammatory features, and imbalance between the different T cell subsets, including Th17 and regulatory T cells (Treg cells). In the thymus from MG patients, Treg cell numbers are normal while their suppressive function is severely defective, and this defect could not be explained by contaminating effector CD127low T cells. A transcriptomic analysis of Treg cell and conventional T cell (Tconv; CD4+CD25− cells) subsets pointed out an upregulation of Th17‐related genes in MG cells. Together with our previous findings of an inflammatory signature in the MG thymus and an overproduction of IL‐1 and IL‐6 by MG thymic epithelial cells (TEC), these data strongly suggest that T cell functions are profoundly altered in the thymic pathological environment. In this short review we discuss the mechanisms of chronic inflammation linked to the pathophysiology of MG disease.</description><identifier>ISSN: 0077-8923</identifier><identifier>EISSN: 1749-6632</identifier><identifier>DOI: 10.1111/j.1749-6632.2012.06791.x</identifier><identifier>PMID: 23252896</identifier><identifier>CODEN: ANYAA9</identifier><language>eng</language><publisher>Malden, USA: Blackwell Publishing Inc</publisher><subject>Epithelial Cells - metabolism ; Humans ; inflammation ; Interleukin-1 - metabolism ; Interleukin-17 - metabolism ; Interleukin-6 - metabolism ; Life Sciences ; Lymphocytes ; myasthenia gravis ; Myasthenia Gravis - immunology ; Myasthenia Gravis - pathology ; T cell receptors ; T-Lymphocytes, Regulatory - metabolism ; T-Lymphocytes, Regulatory - pathology ; Th17 ; thymic epithelial cells ; thymus ; Treg cells</subject><ispartof>Annals of the New York Academy of Sciences, 2012-12, Vol.1274 (1), p.40-47</ispartof><rights>2012 New York Academy of Sciences.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5031-71a8f1dc787797afd30e707b7a30af2e74800410d7d9c2f0f0c6c23a281a6a9b3</citedby><cites>FETCH-LOGICAL-c5031-71a8f1dc787797afd30e707b7a30af2e74800410d7d9c2f0f0c6c23a281a6a9b3</cites><orcidid>0000-0001-7522-5974</orcidid></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.1749-6632.2012.06791.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1749-6632.2012.06791.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,781,785,886,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23252896$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-03442113$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Gradolatto, Angeline</creatorcontrib><creatorcontrib>Nazzal, Dani</creatorcontrib><creatorcontrib>Foti, Maria</creatorcontrib><creatorcontrib>Bismuth, Jacky</creatorcontrib><creatorcontrib>Truffault, Frederique</creatorcontrib><creatorcontrib>Panse, Rozen Le</creatorcontrib><creatorcontrib>Berrih-Aknin, Sonia</creatorcontrib><title>Defects of immunoregulatory mechanisms in myasthenia gravis: role of IL-17</title><title>Annals of the New York Academy of Sciences</title><addtitle>Ann N Y Acad Sci</addtitle><description>Deficient immunoregulation is consistently observed in autoimmune diseases. Here, we summarize the abnormalities of the T cell response in autoimmune myasthenia gravis (MG) by focusing on activation markers, inflammatory features, and imbalance between the different T cell subsets, including Th17 and regulatory T cells (Treg cells). In the thymus from MG patients, Treg cell numbers are normal while their suppressive function is severely defective, and this defect could not be explained by contaminating effector CD127low T cells. A transcriptomic analysis of Treg cell and conventional T cell (Tconv; CD4+CD25− cells) subsets pointed out an upregulation of Th17‐related genes in MG cells. Together with our previous findings of an inflammatory signature in the MG thymus and an overproduction of IL‐1 and IL‐6 by MG thymic epithelial cells (TEC), these data strongly suggest that T cell functions are profoundly altered in the thymic pathological environment. In this short review we discuss the mechanisms of chronic inflammation linked to the pathophysiology of MG disease.</description><subject>Epithelial Cells - metabolism</subject><subject>Humans</subject><subject>inflammation</subject><subject>Interleukin-1 - metabolism</subject><subject>Interleukin-17 - metabolism</subject><subject>Interleukin-6 - metabolism</subject><subject>Life Sciences</subject><subject>Lymphocytes</subject><subject>myasthenia gravis</subject><subject>Myasthenia Gravis - immunology</subject><subject>Myasthenia Gravis - pathology</subject><subject>T cell receptors</subject><subject>T-Lymphocytes, Regulatory - metabolism</subject><subject>T-Lymphocytes, Regulatory - pathology</subject><subject>Th17</subject><subject>thymic epithelial cells</subject><subject>thymus</subject><subject>Treg cells</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9v0zAUxy0EYmXwL6BIXOCQ4GcnfjYHpDJgHSrjQBniZLmps7rkx7CT0f73OGT0wGm-2Hr-vO-z9SEkAZpBXK93GWCuUiE4yxgFllGBCrL9AzI7XjwkM0oRU6kYPyFPQtjRSMocH5MTxlnBpBIz8um9rWzZh6SrEtc0Q9t5ez3Upu_8IWlsuTWtC01IXJs0BxP6rW2dSa69uXXhTeK72o6dF8sU8Cl5VJk62Gd3-yn59vHD6myRLr-cX5zNl2lZUA4pgpEVbEqUiApNteHUIsU1Gk5NxSzmktIc6AY3qmQVrWgpSsYNk2CEUWt-Sl5NuVtT6xvvGuMPujNOL-ZLPdYoz3MGwG8hsi8n9sZ3vwYbet24UNq6Nq3thqCBIWeAhczvgzKkikMR0Rf_obtu8G38tAYUSinKpIiUnKjSdyF4Wx0fC1SPGvVOj7b0aEuPGvVfjXofW5_fDRjWjd0cG_95i8DbCfjtanu4d7C-_DH_Oh5jQDoFuNDb_THA-J9aIMdCf7881-9WK3G1-HwV5_4BI0-3mQ</recordid><startdate>201212</startdate><enddate>201212</enddate><creator>Gradolatto, Angeline</creator><creator>Nazzal, Dani</creator><creator>Foti, Maria</creator><creator>Bismuth, Jacky</creator><creator>Truffault, Frederique</creator><creator>Panse, Rozen Le</creator><creator>Berrih-Aknin, Sonia</creator><general>Blackwell Publishing Inc</general><general>Wiley Subscription Services, Inc</general><general>Wiley</general><scope>BSCLL</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7ST</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>SOI</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0001-7522-5974</orcidid></search><sort><creationdate>201212</creationdate><title>Defects of immunoregulatory mechanisms in myasthenia gravis: role of IL-17</title><author>Gradolatto, Angeline ; 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Here, we summarize the abnormalities of the T cell response in autoimmune myasthenia gravis (MG) by focusing on activation markers, inflammatory features, and imbalance between the different T cell subsets, including Th17 and regulatory T cells (Treg cells). In the thymus from MG patients, Treg cell numbers are normal while their suppressive function is severely defective, and this defect could not be explained by contaminating effector CD127low T cells. A transcriptomic analysis of Treg cell and conventional T cell (Tconv; CD4+CD25− cells) subsets pointed out an upregulation of Th17‐related genes in MG cells. Together with our previous findings of an inflammatory signature in the MG thymus and an overproduction of IL‐1 and IL‐6 by MG thymic epithelial cells (TEC), these data strongly suggest that T cell functions are profoundly altered in the thymic pathological environment. In this short review we discuss the mechanisms of chronic inflammation linked to the pathophysiology of MG disease.</abstract><cop>Malden, USA</cop><pub>Blackwell Publishing Inc</pub><pmid>23252896</pmid><doi>10.1111/j.1749-6632.2012.06791.x</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-7522-5974</orcidid></addata></record> |
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| ispartof | Annals of the New York Academy of Sciences, 2012-12, Vol.1274 (1), p.40-47 |
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| subjects | Epithelial Cells - metabolism Humans inflammation Interleukin-1 - metabolism Interleukin-17 - metabolism Interleukin-6 - metabolism Life Sciences Lymphocytes myasthenia gravis Myasthenia Gravis - immunology Myasthenia Gravis - pathology T cell receptors T-Lymphocytes, Regulatory - metabolism T-Lymphocytes, Regulatory - pathology Th17 thymic epithelial cells thymus Treg cells |
| title | Defects of immunoregulatory mechanisms in myasthenia gravis: role of IL-17 |
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