Characterization of T-Cell Receptor Repertoire in Patients with Rheumatoid Arthritis Receiving Biologic Therapies
Rheumatoid arthritis (RA) is a systematic autoimmune disease, predominantly causing chronic polyarticular inflammation and joint injury of patients. For the treatment of RA, biologic disease-modifying antirheumatic drugs (bDMARDs) have been used to reduce inflammation and to interfere with disease p...
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| Veröffentlicht in: | Disease markers 2019, Vol.2019 (2019), p.1-12 |
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| creator | Chang, Wei Chiao Liu, Xiao Wei, James Cheng-Chung Wong, Henry Sung-Ching Hsu, Yu-Wen Chang, Che-Mai Liao, Hsien-Tzung |
| description | Rheumatoid arthritis (RA) is a systematic autoimmune disease, predominantly causing chronic polyarticular inflammation and joint injury of patients. For the treatment of RA, biologic disease-modifying antirheumatic drugs (bDMARDs) have been used to reduce inflammation and to interfere with disease progression through targeting and mediating the immune system. Although the therapeutic effects of bDMARDs in RA patients have been widely reported, whether these drugs also play important roles in T-cell repertoire status is still unclear. We therefore designed the study to identify the role of T-cell repertoire profiles in RA patients with different types of bDMARD treatments. A high-throughput sequencing approach was applied to profile the T-cell receptor beta chain (TCRB) repertoire of circulating T lymphocytes in eight patients given adalimumab (anti-TNF-α) with/without the following use of either rituximab (anti-CD20) or tocilizumab (anti-IL6R). We subsequently analyzed discrepancies in the clonal diversity and CDR3 length distribution as well as usages of the V and J genes of TCRB repertoire and interrogated the association between repertoire diversity and disease activities followed by the treatment of bDMARDs in these RA patients. All groups of patients showed well-controlled DAS28 scores ( |
| doi_str_mv | 10.1155/2019/2364943 |
| format | Article |
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For the treatment of RA, biologic disease-modifying antirheumatic drugs (bDMARDs) have been used to reduce inflammation and to interfere with disease progression through targeting and mediating the immune system. Although the therapeutic effects of bDMARDs in RA patients have been widely reported, whether these drugs also play important roles in T-cell repertoire status is still unclear. We therefore designed the study to identify the role of T-cell repertoire profiles in RA patients with different types of bDMARD treatments. A high-throughput sequencing approach was applied to profile the T-cell receptor beta chain (TCRB) repertoire of circulating T lymphocytes in eight patients given adalimumab (anti-TNF-α) with/without the following use of either rituximab (anti-CD20) or tocilizumab (anti-IL6R). We subsequently analyzed discrepancies in the clonal diversity and CDR3 length distribution as well as usages of the V and J genes of TCRB repertoire and interrogated the association between repertoire diversity and disease activities followed by the treatment of bDMARDs in these RA patients. All groups of patients showed well-controlled DAS28 scores (<2.6) after different treatment regimens of drugs and displayed no significant statistical differences in repertoire diversity, distribution of CDR3 lengths, and usage of V and J genes of TCRB. Nonetheless, a trend between overall TCRB repertoire diversity and disease activity scores in all bDMARD-treated RA patients was observed. Additionally, age was found to be associated with repertoire diversity in RA patients treated with bDMARDs. Through the profiling of the TCR repertoire in RA patients receiving different biologic medications, our study indicated an inverse tendency between TCR repertoire diversity and disease activity after biologic treatment in RA patients.</description><identifier>ISSN: 0278-0240</identifier><identifier>EISSN: 1875-8630</identifier><identifier>DOI: 10.1155/2019/2364943</identifier><identifier>PMID: 31360262</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Adalimumab ; Adult ; Aged ; Antirheumatic Agents - therapeutic use ; Arthritis ; Arthritis, Rheumatoid - drug therapy ; Arthritis, Rheumatoid - metabolism ; Arthritis, Rheumatoid - pathology ; Autoimmune diseases ; B cells ; Biodiversity ; Biological Therapy - methods ; Biomarkers - analysis ; Care and treatment ; Case-Control Studies ; CD20 antigen ; Complementarity-determining region 3 ; Cytokines ; Development and progression ; Disease Progression ; Drugs ; Female ; Follow-Up Studies ; Genes ; Health aspects ; Humans ; Immune system ; Immunology ; Immunosuppressive agents ; Inflammation ; Interleukin 6 ; Interleukin 6 receptors ; Lymphocytes ; Lymphocytes T ; Male ; Medical treatment ; Middle Aged ; Monoclonal antibodies ; Next-generation sequencing ; Pathogenesis ; Prognosis ; Receptors, Antigen, T-Cell - genetics ; Receptors, Antigen, T-Cell - metabolism ; Rheumatoid arthritis ; Rheumatoid factor ; Rheumatology ; Rituximab ; Statistical analysis ; T cell receptors ; T cells ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor necrosis factor-α</subject><ispartof>Disease markers, 2019, Vol.2019 (2019), p.1-12</ispartof><rights>Copyright © 2019 Che-Mai Chang et al.</rights><rights>COPYRIGHT 2019 John Wiley & Sons, Inc.</rights><rights>Copyright © 2019 Che-Mai Chang et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Che-Mai Chang et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-fcd1872ae72f9d82c9ded78449f5849bb916a9cb4e65c86ac78c2a77663445773</citedby><cites>FETCH-LOGICAL-c499t-fcd1872ae72f9d82c9ded78449f5849bb916a9cb4e65c86ac78c2a77663445773</cites><orcidid>0000-0002-0353-9744 ; 0000-0002-1235-0679 ; 0000-0002-8573-5924 ; 0000-0001-5930-4840</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/PMC6642763/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6642763/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,4012,27906,27907,27908,53774,53776</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31360262$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Knaś, Małgorzata</contributor><contributor>Małgorzata Knaś</contributor><creatorcontrib>Chang, Wei Chiao</creatorcontrib><creatorcontrib>Liu, Xiao</creatorcontrib><creatorcontrib>Wei, James Cheng-Chung</creatorcontrib><creatorcontrib>Wong, Henry Sung-Ching</creatorcontrib><creatorcontrib>Hsu, Yu-Wen</creatorcontrib><creatorcontrib>Chang, Che-Mai</creatorcontrib><creatorcontrib>Liao, Hsien-Tzung</creatorcontrib><title>Characterization of T-Cell Receptor Repertoire in Patients with Rheumatoid Arthritis Receiving Biologic Therapies</title><title>Disease markers</title><addtitle>Dis Markers</addtitle><description>Rheumatoid arthritis (RA) is a systematic autoimmune disease, predominantly causing chronic polyarticular inflammation and joint injury of patients. For the treatment of RA, biologic disease-modifying antirheumatic drugs (bDMARDs) have been used to reduce inflammation and to interfere with disease progression through targeting and mediating the immune system. Although the therapeutic effects of bDMARDs in RA patients have been widely reported, whether these drugs also play important roles in T-cell repertoire status is still unclear. We therefore designed the study to identify the role of T-cell repertoire profiles in RA patients with different types of bDMARD treatments. A high-throughput sequencing approach was applied to profile the T-cell receptor beta chain (TCRB) repertoire of circulating T lymphocytes in eight patients given adalimumab (anti-TNF-α) with/without the following use of either rituximab (anti-CD20) or tocilizumab (anti-IL6R). We subsequently analyzed discrepancies in the clonal diversity and CDR3 length distribution as well as usages of the V and J genes of TCRB repertoire and interrogated the association between repertoire diversity and disease activities followed by the treatment of bDMARDs in these RA patients. All groups of patients showed well-controlled DAS28 scores (<2.6) after different treatment regimens of drugs and displayed no significant statistical differences in repertoire diversity, distribution of CDR3 lengths, and usage of V and J genes of TCRB. Nonetheless, a trend between overall TCRB repertoire diversity and disease activity scores in all bDMARD-treated RA patients was observed. Additionally, age was found to be associated with repertoire diversity in RA patients treated with bDMARDs. Through the profiling of the TCR repertoire in RA patients receiving different biologic medications, our study indicated an inverse tendency between TCR repertoire diversity and disease activity after biologic treatment in RA patients.</description><subject>Adalimumab</subject><subject>Adult</subject><subject>Aged</subject><subject>Antirheumatic Agents - therapeutic use</subject><subject>Arthritis</subject><subject>Arthritis, Rheumatoid - drug therapy</subject><subject>Arthritis, Rheumatoid - metabolism</subject><subject>Arthritis, Rheumatoid - pathology</subject><subject>Autoimmune diseases</subject><subject>B cells</subject><subject>Biodiversity</subject><subject>Biological Therapy - methods</subject><subject>Biomarkers - analysis</subject><subject>Care and treatment</subject><subject>Case-Control Studies</subject><subject>CD20 antigen</subject><subject>Complementarity-determining region 3</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Disease Progression</subject><subject>Drugs</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Genes</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Immune system</subject><subject>Immunology</subject><subject>Immunosuppressive agents</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Interleukin 6 receptors</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Medical treatment</subject><subject>Middle Aged</subject><subject>Monoclonal antibodies</subject><subject>Next-generation sequencing</subject><subject>Pathogenesis</subject><subject>Prognosis</subject><subject>Receptors, Antigen, T-Cell - genetics</subject><subject>Receptors, Antigen, T-Cell - metabolism</subject><subject>Rheumatoid arthritis</subject><subject>Rheumatoid factor</subject><subject>Rheumatology</subject><subject>Rituximab</subject><subject>Statistical analysis</subject><subject>T cell receptors</subject><subject>T cells</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor necrosis factor-α</subject><issn>0278-0240</issn><issn>1875-8630</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><recordid>eNqN0c1v0zAYBnALgVgZ3DgjS1yQIMxfsePLpFLxJU0CTeVsuc6bxlMaZ7azCf56XFo24MQplvzzE79-EHpOyVtK6_qMEarPGJdCC_4ALWij6qqRnDxEC8JUUxEmyAl6ktIVIZRpoR-jE065JEyyBbpe9TZalyH6Hzb7MOLQ4XW1gmHAl-BgyiGWxQQxBx8B-xF_LQ7GnPCtzz2-7GHe2bLZ4mXMffTZp18n_Y0ft_idD0PYeofXPUQ7eUhP0aPODgmeHb-n6NuH9-vVp-riy8fPq-VF5YTWuepcW0ZhFhTrdNswp1toVSOE7upG6M1GU2m12wiQtWukdapxzColJReiVoqfovND7jRvdtC6cuVoBzNFv7PxuwnWm793Rt-bbbgxUgqmJC8Br44BMVzPkLLZ-eTKw9gRwpwMY1IRKmlDCn35D70KcxzLeHtFKadMsXu1tQMYP3ah_NftQ82y1MFlLZko6s1BuRhSitDdXZkSs2_c7Bs3x8YLf_HnmHf4d8UFvD6A3o-tvfX_GQfFQGfvNRVSi5r_BCHHvV4</recordid><startdate>2019</startdate><enddate>2019</enddate><creator>Chang, Wei Chiao</creator><creator>Liu, Xiao</creator><creator>Wei, James Cheng-Chung</creator><creator>Wong, Henry Sung-Ching</creator><creator>Hsu, Yu-Wen</creator><creator>Chang, Che-Mai</creator><creator>Liao, Hsien-Tzung</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7QL</scope><scope>7QO</scope><scope>7TK</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0353-9744</orcidid><orcidid>https://orcid.org/0000-0002-1235-0679</orcidid><orcidid>https://orcid.org/0000-0002-8573-5924</orcidid><orcidid>https://orcid.org/0000-0001-5930-4840</orcidid></search><sort><creationdate>2019</creationdate><title>Characterization of T-Cell Receptor Repertoire in Patients with Rheumatoid Arthritis Receiving Biologic Therapies</title><author>Chang, Wei Chiao ; Liu, Xiao ; Wei, James Cheng-Chung ; Wong, Henry Sung-Ching ; Hsu, Yu-Wen ; Chang, Che-Mai ; Liao, Hsien-Tzung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-fcd1872ae72f9d82c9ded78449f5849bb916a9cb4e65c86ac78c2a77663445773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adalimumab</topic><topic>Adult</topic><topic>Aged</topic><topic>Antirheumatic Agents - therapeutic use</topic><topic>Arthritis</topic><topic>Arthritis, Rheumatoid - drug therapy</topic><topic>Arthritis, Rheumatoid - metabolism</topic><topic>Arthritis, Rheumatoid - pathology</topic><topic>Autoimmune diseases</topic><topic>B cells</topic><topic>Biodiversity</topic><topic>Biological Therapy - methods</topic><topic>Biomarkers - analysis</topic><topic>Care and treatment</topic><topic>Case-Control Studies</topic><topic>CD20 antigen</topic><topic>Complementarity-determining region 3</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Disease Progression</topic><topic>Drugs</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Genes</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Immune system</topic><topic>Immunology</topic><topic>Immunosuppressive agents</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Interleukin 6 receptors</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Medical treatment</topic><topic>Middle Aged</topic><topic>Monoclonal antibodies</topic><topic>Next-generation sequencing</topic><topic>Pathogenesis</topic><topic>Prognosis</topic><topic>Receptors, Antigen, T-Cell - genetics</topic><topic>Receptors, Antigen, T-Cell - metabolism</topic><topic>Rheumatoid arthritis</topic><topic>Rheumatoid factor</topic><topic>Rheumatology</topic><topic>Rituximab</topic><topic>Statistical analysis</topic><topic>T cell receptors</topic><topic>T cells</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chang, Wei Chiao</creatorcontrib><creatorcontrib>Liu, Xiao</creatorcontrib><creatorcontrib>Wei, James Cheng-Chung</creatorcontrib><creatorcontrib>Wong, Henry Sung-Ching</creatorcontrib><creatorcontrib>Hsu, Yu-Wen</creatorcontrib><creatorcontrib>Chang, Che-Mai</creatorcontrib><creatorcontrib>Liao, Hsien-Tzung</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Disease markers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chang, Wei Chiao</au><au>Liu, Xiao</au><au>Wei, James Cheng-Chung</au><au>Wong, Henry Sung-Ching</au><au>Hsu, Yu-Wen</au><au>Chang, Che-Mai</au><au>Liao, Hsien-Tzung</au><au>Knaś, Małgorzata</au><au>Małgorzata Knaś</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Characterization of T-Cell Receptor Repertoire in Patients with Rheumatoid Arthritis Receiving Biologic Therapies</atitle><jtitle>Disease markers</jtitle><addtitle>Dis Markers</addtitle><date>2019</date><risdate>2019</risdate><volume>2019</volume><issue>2019</issue><spage>1</spage><epage>12</epage><pages>1-12</pages><issn>0278-0240</issn><eissn>1875-8630</eissn><abstract>Rheumatoid arthritis (RA) is a systematic autoimmune disease, predominantly causing chronic polyarticular inflammation and joint injury of patients. For the treatment of RA, biologic disease-modifying antirheumatic drugs (bDMARDs) have been used to reduce inflammation and to interfere with disease progression through targeting and mediating the immune system. Although the therapeutic effects of bDMARDs in RA patients have been widely reported, whether these drugs also play important roles in T-cell repertoire status is still unclear. We therefore designed the study to identify the role of T-cell repertoire profiles in RA patients with different types of bDMARD treatments. A high-throughput sequencing approach was applied to profile the T-cell receptor beta chain (TCRB) repertoire of circulating T lymphocytes in eight patients given adalimumab (anti-TNF-α) with/without the following use of either rituximab (anti-CD20) or tocilizumab (anti-IL6R). We subsequently analyzed discrepancies in the clonal diversity and CDR3 length distribution as well as usages of the V and J genes of TCRB repertoire and interrogated the association between repertoire diversity and disease activities followed by the treatment of bDMARDs in these RA patients. All groups of patients showed well-controlled DAS28 scores (<2.6) after different treatment regimens of drugs and displayed no significant statistical differences in repertoire diversity, distribution of CDR3 lengths, and usage of V and J genes of TCRB. Nonetheless, a trend between overall TCRB repertoire diversity and disease activity scores in all bDMARD-treated RA patients was observed. Additionally, age was found to be associated with repertoire diversity in RA patients treated with bDMARDs. Through the profiling of the TCR repertoire in RA patients receiving different biologic medications, our study indicated an inverse tendency between TCR repertoire diversity and disease activity after biologic treatment in RA patients.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>31360262</pmid><doi>10.1155/2019/2364943</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-0353-9744</orcidid><orcidid>https://orcid.org/0000-0002-1235-0679</orcidid><orcidid>https://orcid.org/0000-0002-8573-5924</orcidid><orcidid>https://orcid.org/0000-0001-5930-4840</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley Online Library Open Access; PubMed Central; Alma/SFX Local Collection |
| subjects | Adalimumab Adult Aged Antirheumatic Agents - therapeutic use Arthritis Arthritis, Rheumatoid - drug therapy Arthritis, Rheumatoid - metabolism Arthritis, Rheumatoid - pathology Autoimmune diseases B cells Biodiversity Biological Therapy - methods Biomarkers - analysis Care and treatment Case-Control Studies CD20 antigen Complementarity-determining region 3 Cytokines Development and progression Disease Progression Drugs Female Follow-Up Studies Genes Health aspects Humans Immune system Immunology Immunosuppressive agents Inflammation Interleukin 6 Interleukin 6 receptors Lymphocytes Lymphocytes T Male Medical treatment Middle Aged Monoclonal antibodies Next-generation sequencing Pathogenesis Prognosis Receptors, Antigen, T-Cell - genetics Receptors, Antigen, T-Cell - metabolism Rheumatoid arthritis Rheumatoid factor Rheumatology Rituximab Statistical analysis T cell receptors T cells Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor necrosis factor-α |
| title | Characterization of T-Cell Receptor Repertoire in Patients with Rheumatoid Arthritis Receiving Biologic Therapies |
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