Rheumatoid Arthritis-Specific Autoimmunity in the Lung Before and at the Onset of Disease
The lung is implicated as a site for breach of tolerance prior to onset of seropositive rheumatoid arthritis (RA). To substantiate this, we investigated lung-resident B cells in bronchoalveolar lavage (BAL) samples from untreated early RA patients and anti-citrullinated protein antibody (ACPA)-posit...
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| Veröffentlicht in: | Arthritis & rheumatology (Hoboken, N.J.) N.J.), 2023-11, Vol.75 (11), p.1910-1922 |
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| creator | Joshua, Vijay Loberg Haarhaus, Malena Hensvold, Aase Wähämaa, Heidi Gerstner, Christina Hansson, Monika Israelsson, Lena Stålesen, Ragnhild Sköld, Magnus Grunewald, Johan Klareskog, Lars Grönwall, Caroline Réthi, Bence Catrina, Anca Malmström, Vivianne |
| description | The lung is implicated as a site for breach of tolerance prior to onset of seropositive rheumatoid arthritis (RA). To substantiate this, we investigated lung-resident B cells in bronchoalveolar lavage (BAL) samples from untreated early RA patients and anti-citrullinated protein antibody (ACPA)-positive individuals at risk for developing RA.
Single B cells (n = 7,680) were phenotyped and isolated from BAL samples from individuals at risk of RA (n = 3) and at RA diagnosis (n = 9). The immunoglobulin variable region transcripts were sequenced and selected for expression as monoclonal antibodies (n = 141). Monoclonal ACPAs were tested for reactivity patterns and binding to neutrophils.
Using our single-cell approach, we found significantly increased proportions of B lymphocytes in ACPA+ compared to ACPA- individuals. Memory and double-negative B cells were prominent in all subgroups. Upon antibody re-expression, 7 highly mutated citrulline-autoreactive clones originating from different memory B cell subsets were identified, both in individuals at risk of RA and early RA patients. Lung IgG variable gene transcripts from ACPA+ individuals carried frequent mutation-induced N-linked Fab glycosylation sites (P |
| doi_str_mv | 10.1002/art.42549 |
| format | Article |
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Single B cells (n = 7,680) were phenotyped and isolated from BAL samples from individuals at risk of RA (n = 3) and at RA diagnosis (n = 9). The immunoglobulin variable region transcripts were sequenced and selected for expression as monoclonal antibodies (n = 141). Monoclonal ACPAs were tested for reactivity patterns and binding to neutrophils.
Using our single-cell approach, we found significantly increased proportions of B lymphocytes in ACPA+ compared to ACPA- individuals. Memory and double-negative B cells were prominent in all subgroups. Upon antibody re-expression, 7 highly mutated citrulline-autoreactive clones originating from different memory B cell subsets were identified, both in individuals at risk of RA and early RA patients. Lung IgG variable gene transcripts from ACPA+ individuals carried frequent mutation-induced N-linked Fab glycosylation sites (P < 0.001), often in the framework 3 of the variable region. Two of the lung ACPAs bound to activated neutrophils, 1 from an individual at risk of RA and 1 from an early RA patient.
T cell-driven B cell differentiation resulting in local class switching and somatic hypermutation are evident in lungs before as well as in early stages of ACPA+ RA. Our findings add to the notion of lung mucosa being a site for initiation of citrulline autoimmunity preceding seropositive RA.</description><identifier>ISSN: 2326-5191</identifier><identifier>EISSN: 2326-5205</identifier><identifier>DOI: 10.1002/art.42549</identifier><identifier>PMID: 37192126</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Arthritis ; Autoimmune diseases ; Autoimmunity ; Bronchus ; Cell differentiation ; Citrulline ; Class switching ; Differentiation (biology) ; Glycosylation ; Immunoglobulin G ; Immunological memory ; Immunological tolerance ; Lavage ; Leukocytes (neutrophilic) ; Lung diseases ; Lungs ; Lymphocytes ; Lymphocytes B ; Lymphocytes T ; Memory cells ; Monoclonal antibodies ; Neutrophils ; Rheumatoid arthritis ; Risk ; Somatic hypermutation ; Subgroups ; Variable region</subject><ispartof>Arthritis & rheumatology (Hoboken, N.J.), 2023-11, Vol.75 (11), p.1910-1922</ispartof><rights>2023 The Authors. Arthritis & Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology.</rights><rights>2023. This article is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-49ab0197af981f16ebce5cca7a40be5cd223ad12de89188fb7b1ed6eb109a3683</citedby><cites>FETCH-LOGICAL-c386t-49ab0197af981f16ebce5cca7a40be5cd223ad12de89188fb7b1ed6eb109a3683</cites><orcidid>0000-0001-9251-8082 ; 0000-0001-8220-5015 ; 0000-0002-2606-8180 ; 0000-0002-7669-3777 ; 0000-0002-9111-5537</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,550,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37192126$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:153464703$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Joshua, Vijay</creatorcontrib><creatorcontrib>Loberg Haarhaus, Malena</creatorcontrib><creatorcontrib>Hensvold, Aase</creatorcontrib><creatorcontrib>Wähämaa, Heidi</creatorcontrib><creatorcontrib>Gerstner, Christina</creatorcontrib><creatorcontrib>Hansson, Monika</creatorcontrib><creatorcontrib>Israelsson, Lena</creatorcontrib><creatorcontrib>Stålesen, Ragnhild</creatorcontrib><creatorcontrib>Sköld, Magnus</creatorcontrib><creatorcontrib>Grunewald, Johan</creatorcontrib><creatorcontrib>Klareskog, Lars</creatorcontrib><creatorcontrib>Grönwall, Caroline</creatorcontrib><creatorcontrib>Réthi, Bence</creatorcontrib><creatorcontrib>Catrina, Anca</creatorcontrib><creatorcontrib>Malmström, Vivianne</creatorcontrib><title>Rheumatoid Arthritis-Specific Autoimmunity in the Lung Before and at the Onset of Disease</title><title>Arthritis & rheumatology (Hoboken, N.J.)</title><addtitle>Arthritis Rheumatol</addtitle><description>The lung is implicated as a site for breach of tolerance prior to onset of seropositive rheumatoid arthritis (RA). To substantiate this, we investigated lung-resident B cells in bronchoalveolar lavage (BAL) samples from untreated early RA patients and anti-citrullinated protein antibody (ACPA)-positive individuals at risk for developing RA.
Single B cells (n = 7,680) were phenotyped and isolated from BAL samples from individuals at risk of RA (n = 3) and at RA diagnosis (n = 9). The immunoglobulin variable region transcripts were sequenced and selected for expression as monoclonal antibodies (n = 141). Monoclonal ACPAs were tested for reactivity patterns and binding to neutrophils.
Using our single-cell approach, we found significantly increased proportions of B lymphocytes in ACPA+ compared to ACPA- individuals. Memory and double-negative B cells were prominent in all subgroups. Upon antibody re-expression, 7 highly mutated citrulline-autoreactive clones originating from different memory B cell subsets were identified, both in individuals at risk of RA and early RA patients. Lung IgG variable gene transcripts from ACPA+ individuals carried frequent mutation-induced N-linked Fab glycosylation sites (P < 0.001), often in the framework 3 of the variable region. Two of the lung ACPAs bound to activated neutrophils, 1 from an individual at risk of RA and 1 from an early RA patient.
T cell-driven B cell differentiation resulting in local class switching and somatic hypermutation are evident in lungs before as well as in early stages of ACPA+ RA. Our findings add to the notion of lung mucosa being a site for initiation of citrulline autoimmunity preceding seropositive RA.</description><subject>Arthritis</subject><subject>Autoimmune diseases</subject><subject>Autoimmunity</subject><subject>Bronchus</subject><subject>Cell differentiation</subject><subject>Citrulline</subject><subject>Class switching</subject><subject>Differentiation (biology)</subject><subject>Glycosylation</subject><subject>Immunoglobulin G</subject><subject>Immunological memory</subject><subject>Immunological tolerance</subject><subject>Lavage</subject><subject>Leukocytes (neutrophilic)</subject><subject>Lung diseases</subject><subject>Lungs</subject><subject>Lymphocytes</subject><subject>Lymphocytes B</subject><subject>Lymphocytes T</subject><subject>Memory cells</subject><subject>Monoclonal antibodies</subject><subject>Neutrophils</subject><subject>Rheumatoid arthritis</subject><subject>Risk</subject><subject>Somatic hypermutation</subject><subject>Subgroups</subject><subject>Variable region</subject><issn>2326-5191</issn><issn>2326-5205</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>D8T</sourceid><recordid>eNpd0U1P3DAQBmCrouoiyqF_oLLUCz0EPLaT2McFWkBaCQnaQ0-Wk0y6pptk8YcQ_77eLw744tH40Wisl5AvwM6BMX5hfTyXvJT6AznmgldFyVl5dKhBw4ychvDE8tE1q1j5icxEDZoDr47Jn4clpsHGyXV07uPSu-hC8bjG1vWupfOUX4YhjS6-UjfSuES6SONfeon95JHasaM2btv3Y8BIp55eu4A24GfysbergKf7-4T8_vnj19Vtsbi_ubuaL4pWqCoWUtuGga5trxX0UGHTYtm2traSNbnqOBe2A96h0qBU39QNYJcZMG1FpcQJKXZzwwuuU2PW3g3Wv5rJOrNv_csVGilLXbHsz3Z-7afnhCGawYUWVys74pSC4QqkglKoDf32jj5NyY_5N1kpUUoQkmf1fadaP4XgsX9bAZjZRGRyRGYbUbZf9xNTM2D3Jg-BiP-2XIvf</recordid><startdate>20231101</startdate><enddate>20231101</enddate><creator>Joshua, Vijay</creator><creator>Loberg Haarhaus, Malena</creator><creator>Hensvold, Aase</creator><creator>Wähämaa, Heidi</creator><creator>Gerstner, Christina</creator><creator>Hansson, Monika</creator><creator>Israelsson, Lena</creator><creator>Stålesen, Ragnhild</creator><creator>Sköld, Magnus</creator><creator>Grunewald, Johan</creator><creator>Klareskog, Lars</creator><creator>Grönwall, Caroline</creator><creator>Réthi, Bence</creator><creator>Catrina, Anca</creator><creator>Malmström, Vivianne</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TM</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope><orcidid>https://orcid.org/0000-0001-9251-8082</orcidid><orcidid>https://orcid.org/0000-0001-8220-5015</orcidid><orcidid>https://orcid.org/0000-0002-2606-8180</orcidid><orcidid>https://orcid.org/0000-0002-7669-3777</orcidid><orcidid>https://orcid.org/0000-0002-9111-5537</orcidid></search><sort><creationdate>20231101</creationdate><title>Rheumatoid Arthritis-Specific Autoimmunity in the Lung Before and at the Onset of Disease</title><author>Joshua, Vijay ; 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To substantiate this, we investigated lung-resident B cells in bronchoalveolar lavage (BAL) samples from untreated early RA patients and anti-citrullinated protein antibody (ACPA)-positive individuals at risk for developing RA.
Single B cells (n = 7,680) were phenotyped and isolated from BAL samples from individuals at risk of RA (n = 3) and at RA diagnosis (n = 9). The immunoglobulin variable region transcripts were sequenced and selected for expression as monoclonal antibodies (n = 141). Monoclonal ACPAs were tested for reactivity patterns and binding to neutrophils.
Using our single-cell approach, we found significantly increased proportions of B lymphocytes in ACPA+ compared to ACPA- individuals. Memory and double-negative B cells were prominent in all subgroups. Upon antibody re-expression, 7 highly mutated citrulline-autoreactive clones originating from different memory B cell subsets were identified, both in individuals at risk of RA and early RA patients. Lung IgG variable gene transcripts from ACPA+ individuals carried frequent mutation-induced N-linked Fab glycosylation sites (P < 0.001), often in the framework 3 of the variable region. Two of the lung ACPAs bound to activated neutrophils, 1 from an individual at risk of RA and 1 from an early RA patient.
T cell-driven B cell differentiation resulting in local class switching and somatic hypermutation are evident in lungs before as well as in early stages of ACPA+ RA. Our findings add to the notion of lung mucosa being a site for initiation of citrulline autoimmunity preceding seropositive RA.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>37192126</pmid><doi>10.1002/art.42549</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-9251-8082</orcidid><orcidid>https://orcid.org/0000-0001-8220-5015</orcidid><orcidid>https://orcid.org/0000-0002-2606-8180</orcidid><orcidid>https://orcid.org/0000-0002-7669-3777</orcidid><orcidid>https://orcid.org/0000-0002-9111-5537</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Arthritis Autoimmune diseases Autoimmunity Bronchus Cell differentiation Citrulline Class switching Differentiation (biology) Glycosylation Immunoglobulin G Immunological memory Immunological tolerance Lavage Leukocytes (neutrophilic) Lung diseases Lungs Lymphocytes Lymphocytes B Lymphocytes T Memory cells Monoclonal antibodies Neutrophils Rheumatoid arthritis Risk Somatic hypermutation Subgroups Variable region |
| title | Rheumatoid Arthritis-Specific Autoimmunity in the Lung Before and at the Onset of Disease |
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