Loading…
Activation of plasmacytoid dendritic cells by apoptotic particles – mechanism for the loss of immunological tolerance in Sjögren's syndrome
Summary Sjögren's syndrome (SS) is a common autoimmune disease targeting salivary and lacrimal glands. It is strongly female‐dominant, characterized by low oestrogen levels combined with a local intracrine dihydrotestosterone defect. We hypothesized that these hormonal deficits lead to increase...
Saved in:
| Published in: | Clinical and experimental immunology 2018-03, Vol.191 (3), p.301-310 |
|---|---|
| Main Authors: | , , , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c4817-2d42284225c42681ac7b42fc7d2f4b3e1373c0150f1fa0461269b7a5dc0ec29d3 |
|---|---|
| cites | cdi_FETCH-LOGICAL-c4817-2d42284225c42681ac7b42fc7d2f4b3e1373c0150f1fa0461269b7a5dc0ec29d3 |
| container_end_page | 310 |
| container_issue | 3 |
| container_start_page | 301 |
| container_title | Clinical and experimental immunology |
| container_volume | 191 |
| creator | Ainola, M. Porola, P. Takakubo, Y. Przybyla, B. Kouri, V. P. Tolvanen, T. A. Hänninen, A. Nordström, D. C. |
| description | Summary
Sjögren's syndrome (SS) is a common autoimmune disease targeting salivary and lacrimal glands. It is strongly female‐dominant, characterized by low oestrogen levels combined with a local intracrine dihydrotestosterone defect. We hypothesized that these hormonal deficits lead to increased apoptosis of the epithelial cells and plasmacytoid dendritic cell (pDC)‐mediated proinflammatory host responses. Expression of Toll‐like receptors (TLRs)‐7 and ‐9 and cytokine profiles was studied in pDCs treated with apoptotic particles collected in consecutive centrifugation steps of media from apoptotic cells. Expression and localization of SS autoantigens in these particles was also analysed. Furthermore, the effects of sex steroids were studied in pDCs cultured with several concentrations of dihydrotestosterone and 17‐β‐oestradiol, and in saliva of patient treated with dehydroepiandrosterone. Apoptosis of the epithelial cells led to cleavage and translocation of SS‐autoantigens, α‐fodrin and SS‐A, into apoptotic particles. The apoptosis‐induced apoptotic particles also contained another SS‐autoantigen, hy1‐RNA. These particles were internalized by pDCs in a size‐dependent manner and affected TLR‐7 and ‐9 expression and the production of proinflammatory cytokines. The analysed androgens protected cells from apoptosis, influenced redistribution of autoantigens and diminished the apoptotic particle‐stimulated increase of the TLRs in pDCs. Our findings suggest that the formation of apoptotic particles may play a role in loss of immune tolerance, manifested by production of autoantibodies and the onset of autoinflammation in SS.
Hormonal deficits in Sjögren's syndrome may lead to increased apoptosis of the epithelial cells and thus plasmacytoid dendritic cell (pDC) mediated pro‐inflammatory host responses. Cell derived apoptotic particles were attached to the surface or taken into pDCs. The intake of apoptotic particles increased TLRs and proinflammatory cytokines in pDCs, but not IFNs, and the effects depend on the size of particles, as apoptotic bodies (1‐4 µm) were mainly secreted in pellet 3 (P3) and microparticles (200‐1000 nm) in pellet 5. |
| doi_str_mv | 10.1111/cei.13077 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5801512</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1961035457</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4817-2d42284225c42681ac7b42fc7d2f4b3e1373c0150f1fa0461269b7a5dc0ec29d3</originalsourceid><addsrcrecordid>eNp1kU9u1DAUhy0EokPbBRdA3gGLtLbjOMkGqRq1UKkSC2BtOc7LjCv_CXamKLseoVIv0FNwgHITToKHKRUssGRZfv70Pev9EHpJyRHN61iDOaIlqesnaEFLURWM8fYpWhBC2qKlhO-hFyld5qsQgj1HeywXKyKaBbo50ZO5UpMJHocBj1Ylp_Q8BdPjHnwfzWQ01mBtwt2M1RjGKWxLo4r5sJDu735e397fOdBr5U1yeAgRT2vANqS0dRrnNj7YsDJaWTwFC1F5Ddh4_Onyx_dVBP864TTnZsHBAXo2KJvg8OHcR1_OTj8vPxQXH9-fL08uCs0bWhes54w1eVeaM9FQpeuOs0HXPRt4VwIt61ITWpGBDopwQZlou1pVvSagWduX--jdzjtuOge9Bj9FZeUYjVNxlkEZ-e-LN2u5CleyarKWsix48yCI4esG0iSdSdtBKQ9hkyRtBSVlxas6o293qI55JhGGxzaUyG2CMicofyeY2Vd__-uR_BNZBo53wDdjYf6_SS5Pz3fKX5V2rFI</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1961035457</pqid></control><display><type>article</type><title>Activation of plasmacytoid dendritic cells by apoptotic particles – mechanism for the loss of immunological tolerance in Sjögren's syndrome</title><source>Wiley-Blackwell Journals</source><source>PubMed</source><source>Oxford Journals Online</source><creator>Ainola, M. ; Porola, P. ; Takakubo, Y. ; Przybyla, B. ; Kouri, V. P. ; Tolvanen, T. A. ; Hänninen, A. ; Nordström, D. C.</creator><creatorcontrib>Ainola, M. ; Porola, P. ; Takakubo, Y. ; Przybyla, B. ; Kouri, V. P. ; Tolvanen, T. A. ; Hänninen, A. ; Nordström, D. C.</creatorcontrib><description>Summary
Sjögren's syndrome (SS) is a common autoimmune disease targeting salivary and lacrimal glands. It is strongly female‐dominant, characterized by low oestrogen levels combined with a local intracrine dihydrotestosterone defect. We hypothesized that these hormonal deficits lead to increased apoptosis of the epithelial cells and plasmacytoid dendritic cell (pDC)‐mediated proinflammatory host responses. Expression of Toll‐like receptors (TLRs)‐7 and ‐9 and cytokine profiles was studied in pDCs treated with apoptotic particles collected in consecutive centrifugation steps of media from apoptotic cells. Expression and localization of SS autoantigens in these particles was also analysed. Furthermore, the effects of sex steroids were studied in pDCs cultured with several concentrations of dihydrotestosterone and 17‐β‐oestradiol, and in saliva of patient treated with dehydroepiandrosterone. Apoptosis of the epithelial cells led to cleavage and translocation of SS‐autoantigens, α‐fodrin and SS‐A, into apoptotic particles. The apoptosis‐induced apoptotic particles also contained another SS‐autoantigen, hy1‐RNA. These particles were internalized by pDCs in a size‐dependent manner and affected TLR‐7 and ‐9 expression and the production of proinflammatory cytokines. The analysed androgens protected cells from apoptosis, influenced redistribution of autoantigens and diminished the apoptotic particle‐stimulated increase of the TLRs in pDCs. Our findings suggest that the formation of apoptotic particles may play a role in loss of immune tolerance, manifested by production of autoantibodies and the onset of autoinflammation in SS.
Hormonal deficits in Sjögren's syndrome may lead to increased apoptosis of the epithelial cells and thus plasmacytoid dendritic cell (pDC) mediated pro‐inflammatory host responses. Cell derived apoptotic particles were attached to the surface or taken into pDCs. The intake of apoptotic particles increased TLRs and proinflammatory cytokines in pDCs, but not IFNs, and the effects depend on the size of particles, as apoptotic bodies (1‐4 µm) were mainly secreted in pellet 3 (P3) and microparticles (200‐1000 nm) in pellet 5.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/cei.13077</identifier><identifier>PMID: 29105068</identifier><language>eng</language><publisher>England: John Wiley and Sons Inc</publisher><subject>Adult ; Aged ; Apoptosis ; autoimmunity ; Carrier Proteins - immunology ; Carrier Proteins - metabolism ; Cell Differentiation ; Cells, Cultured ; cytokines ; Cytokines - metabolism ; dendritic cells ; Dendritic Cells - immunology ; Dihydrotestosterone - metabolism ; Epithelial Cells - immunology ; Epithelial Cells - metabolism ; Estrogens - metabolism ; Extracellular Vesicles - immunology ; Extracellular Vesicles - metabolism ; Female ; Humans ; Immune Tolerance ; Inflammation Mediators - metabolism ; Male ; Microfilament Proteins - immunology ; Microfilament Proteins - metabolism ; Middle Aged ; Original ; Ribonucleoproteins - metabolism ; Salivary Glands - metabolism ; Salivary Glands - pathology ; Sjogren's Syndrome - immunology ; Toll-Like Receptor 7 - genetics ; Toll-Like Receptor 7 - metabolism ; Toll-Like Receptor 9 - genetics ; Toll-Like Receptor 9 - metabolism ; Toll‐like receptors (TLRs) ; Young Adult</subject><ispartof>Clinical and experimental immunology, 2018-03, Vol.191 (3), p.301-310</ispartof><rights>2017 British Society for Immunology</rights><rights>2017 British Society for Immunology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4817-2d42284225c42681ac7b42fc7d2f4b3e1373c0150f1fa0461269b7a5dc0ec29d3</citedby><cites>FETCH-LOGICAL-c4817-2d42284225c42681ac7b42fc7d2f4b3e1373c0150f1fa0461269b7a5dc0ec29d3</cites><orcidid>0000-0003-2853-5851</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%2Fcei.13077$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fcei.13077$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,733,786,790,891,27957,27958,50923,51032,53827,53829</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29105068$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ainola, M.</creatorcontrib><creatorcontrib>Porola, P.</creatorcontrib><creatorcontrib>Takakubo, Y.</creatorcontrib><creatorcontrib>Przybyla, B.</creatorcontrib><creatorcontrib>Kouri, V. P.</creatorcontrib><creatorcontrib>Tolvanen, T. A.</creatorcontrib><creatorcontrib>Hänninen, A.</creatorcontrib><creatorcontrib>Nordström, D. C.</creatorcontrib><title>Activation of plasmacytoid dendritic cells by apoptotic particles – mechanism for the loss of immunological tolerance in Sjögren's syndrome</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>Summary
Sjögren's syndrome (SS) is a common autoimmune disease targeting salivary and lacrimal glands. It is strongly female‐dominant, characterized by low oestrogen levels combined with a local intracrine dihydrotestosterone defect. We hypothesized that these hormonal deficits lead to increased apoptosis of the epithelial cells and plasmacytoid dendritic cell (pDC)‐mediated proinflammatory host responses. Expression of Toll‐like receptors (TLRs)‐7 and ‐9 and cytokine profiles was studied in pDCs treated with apoptotic particles collected in consecutive centrifugation steps of media from apoptotic cells. Expression and localization of SS autoantigens in these particles was also analysed. Furthermore, the effects of sex steroids were studied in pDCs cultured with several concentrations of dihydrotestosterone and 17‐β‐oestradiol, and in saliva of patient treated with dehydroepiandrosterone. Apoptosis of the epithelial cells led to cleavage and translocation of SS‐autoantigens, α‐fodrin and SS‐A, into apoptotic particles. The apoptosis‐induced apoptotic particles also contained another SS‐autoantigen, hy1‐RNA. These particles were internalized by pDCs in a size‐dependent manner and affected TLR‐7 and ‐9 expression and the production of proinflammatory cytokines. The analysed androgens protected cells from apoptosis, influenced redistribution of autoantigens and diminished the apoptotic particle‐stimulated increase of the TLRs in pDCs. Our findings suggest that the formation of apoptotic particles may play a role in loss of immune tolerance, manifested by production of autoantibodies and the onset of autoinflammation in SS.
Hormonal deficits in Sjögren's syndrome may lead to increased apoptosis of the epithelial cells and thus plasmacytoid dendritic cell (pDC) mediated pro‐inflammatory host responses. Cell derived apoptotic particles were attached to the surface or taken into pDCs. The intake of apoptotic particles increased TLRs and proinflammatory cytokines in pDCs, but not IFNs, and the effects depend on the size of particles, as apoptotic bodies (1‐4 µm) were mainly secreted in pellet 3 (P3) and microparticles (200‐1000 nm) in pellet 5.</description><subject>Adult</subject><subject>Aged</subject><subject>Apoptosis</subject><subject>autoimmunity</subject><subject>Carrier Proteins - immunology</subject><subject>Carrier Proteins - metabolism</subject><subject>Cell Differentiation</subject><subject>Cells, Cultured</subject><subject>cytokines</subject><subject>Cytokines - metabolism</subject><subject>dendritic cells</subject><subject>Dendritic Cells - immunology</subject><subject>Dihydrotestosterone - metabolism</subject><subject>Epithelial Cells - immunology</subject><subject>Epithelial Cells - metabolism</subject><subject>Estrogens - metabolism</subject><subject>Extracellular Vesicles - immunology</subject><subject>Extracellular Vesicles - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Immune Tolerance</subject><subject>Inflammation Mediators - metabolism</subject><subject>Male</subject><subject>Microfilament Proteins - immunology</subject><subject>Microfilament Proteins - metabolism</subject><subject>Middle Aged</subject><subject>Original</subject><subject>Ribonucleoproteins - metabolism</subject><subject>Salivary Glands - metabolism</subject><subject>Salivary Glands - pathology</subject><subject>Sjogren's Syndrome - immunology</subject><subject>Toll-Like Receptor 7 - genetics</subject><subject>Toll-Like Receptor 7 - metabolism</subject><subject>Toll-Like Receptor 9 - genetics</subject><subject>Toll-Like Receptor 9 - metabolism</subject><subject>Toll‐like receptors (TLRs)</subject><subject>Young Adult</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kU9u1DAUhy0EokPbBRdA3gGLtLbjOMkGqRq1UKkSC2BtOc7LjCv_CXamKLseoVIv0FNwgHITToKHKRUssGRZfv70Pev9EHpJyRHN61iDOaIlqesnaEFLURWM8fYpWhBC2qKlhO-hFyld5qsQgj1HeywXKyKaBbo50ZO5UpMJHocBj1Ylp_Q8BdPjHnwfzWQ01mBtwt2M1RjGKWxLo4r5sJDu735e397fOdBr5U1yeAgRT2vANqS0dRrnNj7YsDJaWTwFC1F5Ddh4_Onyx_dVBP864TTnZsHBAXo2KJvg8OHcR1_OTj8vPxQXH9-fL08uCs0bWhes54w1eVeaM9FQpeuOs0HXPRt4VwIt61ITWpGBDopwQZlou1pVvSagWduX--jdzjtuOge9Bj9FZeUYjVNxlkEZ-e-LN2u5CleyarKWsix48yCI4esG0iSdSdtBKQ9hkyRtBSVlxas6o293qI55JhGGxzaUyG2CMicofyeY2Vd__-uR_BNZBo53wDdjYf6_SS5Pz3fKX5V2rFI</recordid><startdate>201803</startdate><enddate>201803</enddate><creator>Ainola, M.</creator><creator>Porola, P.</creator><creator>Takakubo, Y.</creator><creator>Przybyla, B.</creator><creator>Kouri, V. P.</creator><creator>Tolvanen, T. A.</creator><creator>Hänninen, A.</creator><creator>Nordström, D. C.</creator><general>John Wiley and Sons Inc</general><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><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2853-5851</orcidid></search><sort><creationdate>201803</creationdate><title>Activation of plasmacytoid dendritic cells by apoptotic particles – mechanism for the loss of immunological tolerance in Sjögren's syndrome</title><author>Ainola, M. ; Porola, P. ; Takakubo, Y. ; Przybyla, B. ; Kouri, V. P. ; Tolvanen, T. A. ; Hänninen, A. ; Nordström, D. C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4817-2d42284225c42681ac7b42fc7d2f4b3e1373c0150f1fa0461269b7a5dc0ec29d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Apoptosis</topic><topic>autoimmunity</topic><topic>Carrier Proteins - immunology</topic><topic>Carrier Proteins - metabolism</topic><topic>Cell Differentiation</topic><topic>Cells, Cultured</topic><topic>cytokines</topic><topic>Cytokines - metabolism</topic><topic>dendritic cells</topic><topic>Dendritic Cells - immunology</topic><topic>Dihydrotestosterone - metabolism</topic><topic>Epithelial Cells - immunology</topic><topic>Epithelial Cells - metabolism</topic><topic>Estrogens - metabolism</topic><topic>Extracellular Vesicles - immunology</topic><topic>Extracellular Vesicles - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Immune Tolerance</topic><topic>Inflammation Mediators - metabolism</topic><topic>Male</topic><topic>Microfilament Proteins - immunology</topic><topic>Microfilament Proteins - metabolism</topic><topic>Middle Aged</topic><topic>Original</topic><topic>Ribonucleoproteins - metabolism</topic><topic>Salivary Glands - metabolism</topic><topic>Salivary Glands - pathology</topic><topic>Sjogren's Syndrome - immunology</topic><topic>Toll-Like Receptor 7 - genetics</topic><topic>Toll-Like Receptor 7 - metabolism</topic><topic>Toll-Like Receptor 9 - genetics</topic><topic>Toll-Like Receptor 9 - metabolism</topic><topic>Toll‐like receptors (TLRs)</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ainola, M.</creatorcontrib><creatorcontrib>Porola, P.</creatorcontrib><creatorcontrib>Takakubo, Y.</creatorcontrib><creatorcontrib>Przybyla, B.</creatorcontrib><creatorcontrib>Kouri, V. P.</creatorcontrib><creatorcontrib>Tolvanen, T. A.</creatorcontrib><creatorcontrib>Hänninen, A.</creatorcontrib><creatorcontrib>Nordström, D. C.</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>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>Ainola, M.</au><au>Porola, P.</au><au>Takakubo, Y.</au><au>Przybyla, B.</au><au>Kouri, V. P.</au><au>Tolvanen, T. A.</au><au>Hänninen, A.</au><au>Nordström, D. C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of plasmacytoid dendritic cells by apoptotic particles – mechanism for the loss of immunological tolerance in Sjögren's syndrome</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2018-03</date><risdate>2018</risdate><volume>191</volume><issue>3</issue><spage>301</spage><epage>310</epage><pages>301-310</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Summary
Sjögren's syndrome (SS) is a common autoimmune disease targeting salivary and lacrimal glands. It is strongly female‐dominant, characterized by low oestrogen levels combined with a local intracrine dihydrotestosterone defect. We hypothesized that these hormonal deficits lead to increased apoptosis of the epithelial cells and plasmacytoid dendritic cell (pDC)‐mediated proinflammatory host responses. Expression of Toll‐like receptors (TLRs)‐7 and ‐9 and cytokine profiles was studied in pDCs treated with apoptotic particles collected in consecutive centrifugation steps of media from apoptotic cells. Expression and localization of SS autoantigens in these particles was also analysed. Furthermore, the effects of sex steroids were studied in pDCs cultured with several concentrations of dihydrotestosterone and 17‐β‐oestradiol, and in saliva of patient treated with dehydroepiandrosterone. Apoptosis of the epithelial cells led to cleavage and translocation of SS‐autoantigens, α‐fodrin and SS‐A, into apoptotic particles. The apoptosis‐induced apoptotic particles also contained another SS‐autoantigen, hy1‐RNA. These particles were internalized by pDCs in a size‐dependent manner and affected TLR‐7 and ‐9 expression and the production of proinflammatory cytokines. The analysed androgens protected cells from apoptosis, influenced redistribution of autoantigens and diminished the apoptotic particle‐stimulated increase of the TLRs in pDCs. Our findings suggest that the formation of apoptotic particles may play a role in loss of immune tolerance, manifested by production of autoantibodies and the onset of autoinflammation in SS.
Hormonal deficits in Sjögren's syndrome may lead to increased apoptosis of the epithelial cells and thus plasmacytoid dendritic cell (pDC) mediated pro‐inflammatory host responses. Cell derived apoptotic particles were attached to the surface or taken into pDCs. The intake of apoptotic particles increased TLRs and proinflammatory cytokines in pDCs, but not IFNs, and the effects depend on the size of particles, as apoptotic bodies (1‐4 µm) were mainly secreted in pellet 3 (P3) and microparticles (200‐1000 nm) in pellet 5.</abstract><cop>England</cop><pub>John Wiley and Sons Inc</pub><pmid>29105068</pmid><doi>10.1111/cei.13077</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-2853-5851</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0009-9104 |
| ispartof | Clinical and experimental immunology, 2018-03, Vol.191 (3), p.301-310 |
| issn | 0009-9104 1365-2249 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5801512 |
| source | Wiley-Blackwell Journals; PubMed; Oxford Journals Online |
| subjects | Adult Aged Apoptosis autoimmunity Carrier Proteins - immunology Carrier Proteins - metabolism Cell Differentiation Cells, Cultured cytokines Cytokines - metabolism dendritic cells Dendritic Cells - immunology Dihydrotestosterone - metabolism Epithelial Cells - immunology Epithelial Cells - metabolism Estrogens - metabolism Extracellular Vesicles - immunology Extracellular Vesicles - metabolism Female Humans Immune Tolerance Inflammation Mediators - metabolism Male Microfilament Proteins - immunology Microfilament Proteins - metabolism Middle Aged Original Ribonucleoproteins - metabolism Salivary Glands - metabolism Salivary Glands - pathology Sjogren's Syndrome - immunology Toll-Like Receptor 7 - genetics Toll-Like Receptor 7 - metabolism Toll-Like Receptor 9 - genetics Toll-Like Receptor 9 - metabolism Toll‐like receptors (TLRs) Young Adult |
| title | Activation of plasmacytoid dendritic cells by apoptotic particles – mechanism for the loss of immunological tolerance in Sjögren's syndrome |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-22T18%3A35%3A31IST&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=Activation%20of%20plasmacytoid%20dendritic%20cells%20by%20apoptotic%20particles%C2%A0%E2%80%93%C2%A0mechanism%20for%20the%20loss%20of%20immunological%20tolerance%20in%20Sj%C3%B6gren's%20syndrome&rft.jtitle=Clinical%20and%20experimental%20immunology&rft.au=Ainola,%20M.&rft.date=2018-03&rft.volume=191&rft.issue=3&rft.spage=301&rft.epage=310&rft.pages=301-310&rft.issn=0009-9104&rft.eissn=1365-2249&rft_id=info:doi/10.1111/cei.13077&rft_dat=%3Cproquest_pubme%3E1961035457%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c4817-2d42284225c42681ac7b42fc7d2f4b3e1373c0150f1fa0461269b7a5dc0ec29d3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1961035457&rft_id=info:pmid/29105068&rfr_iscdi=true |