1700 – B cells and autoantibodies最新文献

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1704 Identifying clusters of longitudinal autoantibody profiles associated with systemic lupus erythematosus disease outcomes 1704确定与系统性红斑狼疮疾病结局相关的纵向自身抗体谱簇
1700 – B cells and autoantibodies Pub Date : 2021-11-01 DOI: 10.1136/lupus-2021-lupus21century.99
M. Choi, Irene K. Chen, A. Clarke, M. Fritzler, K. Buhler, M. Urowitz, J. Hanly, C. Gordon, Y. Pierre, S. Bae, J. Diaz, J. Sánchez-Guerrero, S. Bernatsky, D. Wallace, D. Isenberg, Anisur Rahman, J. Merrill, P. Fortin, D. Gladman, I. Bruce, M. Petri, E. Ginzler, M. Dooley, R. Ramsey‐Goldman, S. Manzi, A. Jonsen, G. Alarcón, R. Vollenhoven, C. Aranow, M. Mackay, G. Ruiz‐Irastorza, Sam Lim, M. Inanç, K. Kalunian, S. Jacobsen, C. Peschken, D. Kamen, A. Askanase, D. Sontag, J. Buyon, K. Costenbader
{"title":"1704 Identifying clusters of longitudinal autoantibody profiles associated with systemic lupus erythematosus disease outcomes","authors":"M. Choi, Irene K. Chen, A. Clarke, M. Fritzler, K. Buhler, M. Urowitz, J. Hanly, C. Gordon, Y. Pierre, S. Bae, J. Diaz, J. Sánchez-Guerrero, S. Bernatsky, D. Wallace, D. Isenberg, Anisur Rahman, J. Merrill, P. Fortin, D. Gladman, I. Bruce, M. Petri, E. Ginzler, M. Dooley, R. Ramsey‐Goldman, S. Manzi, A. Jonsen, G. Alarcón, R. Vollenhoven, C. Aranow, M. Mackay, G. Ruiz‐Irastorza, Sam Lim, M. Inanç, K. Kalunian, S. Jacobsen, C. Peschken, D. Kamen, A. Askanase, D. Sontag, J. Buyon, K. Costenbader","doi":"10.1136/lupus-2021-lupus21century.99","DOIUrl":"https://doi.org/10.1136/lupus-2021-lupus21century.99","url":null,"abstract":"","PeriodicalId":235290,"journal":{"name":"1700 – B cells and autoantibodies","volume":"33 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120963766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
1701 Curli amyloid/DNA complexes from bacterial biofilms break tolerance in murine lupus using T cell-independent and T cell-dependent modalities 1701细菌生物膜中的Curli淀粉样蛋白/DNA复合物通过T细胞非依赖性和T细胞依赖性方式破坏小鼠狼疮的耐受性
1700 – B cells and autoantibodies Pub Date : 2021-11-01 DOI: 10.1136/lupus-2021-lupus21century.96
Michael H Lee, S. Tursi, Lauren K Nicastro, Benjamin L Green, R. Caricchio, Ç. Tükel, S. Gallucci
{"title":"1701 Curli amyloid/DNA complexes from bacterial biofilms break tolerance in murine lupus using T cell-independent and T cell-dependent modalities","authors":"Michael H Lee, S. Tursi, Lauren K Nicastro, Benjamin L Green, R. Caricchio, Ç. Tükel, S. Gallucci","doi":"10.1136/lupus-2021-lupus21century.96","DOIUrl":"https://doi.org/10.1136/lupus-2021-lupus21century.96","url":null,"abstract":"Background Epidemiological studies suggest that bacterial infections promote SLE disease in predisposed individuals, but the underlying mechanisms remain unknown. We have found that a subset of SLE patients has asymptomatic bac-teriuria associated with markers of inflammation and flares, suggesting that chronic exposures to microbial products may trigger flares in lupus. Our labs have shown that the bacterial amyloid curli, expressed in multicellular commun-ities ( biofilms) by many bacteria including E. coli , plays a major role in triggering lupus autoimmunity during infec-tion. Curli amyloid/DNA complexes strongly activate dendritic cells and macrophages. When given systemically, curli/DNA complexes and infections with curli-expressing E. coli trigger production of anti-dsDNA and anti-chroma-tin autoantibodies in lupus prone mice and in wild type mice. This stimulation is diminished in TLR2 or TLR9 deficient mice, suggesting a TLR-mediated activation of innate immunity. We have now focused on the effects of curli/DNA complexes on B cells. DNA complexes biofilms or infected with amyloid for short and long-term studies.","PeriodicalId":235290,"journal":{"name":"1700 – B cells and autoantibodies","volume":"34 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123131297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
1703 Activated PI3Kδ signals compromise plasma cell survival via limiting autophagy and increasing endoplasmic reticulum stress 1703活化的PI3Kδ信号通过限制自噬和增加内质网应激影响浆细胞的存活
1700 – B cells and autoantibodies Pub Date : 2021-11-01 DOI: 10.1136/lupus-2021-lupus21century.98
D. Rawlings, Fahd A. Al Qureshah, Sara Sagadiev, Christopher D. Thouvenel, Shuozhi Liu, Zhaolin Hua, B. Hou, Mridu Acharya, Richard G. James
{"title":"1703 Activated PI3Kδ signals compromise plasma cell survival via limiting autophagy and increasing endoplasmic reticulum stress","authors":"D. Rawlings, Fahd A. Al Qureshah, Sara Sagadiev, Christopher D. Thouvenel, Shuozhi Liu, Zhaolin Hua, B. Hou, Mridu Acharya, Richard G. James","doi":"10.1136/lupus-2021-lupus21century.98","DOIUrl":"https://doi.org/10.1136/lupus-2021-lupus21century.98","url":null,"abstract":"","PeriodicalId":235290,"journal":{"name":"1700 – B cells and autoantibodies","volume":"22 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122309879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
1705 Protein assemblages are newly described intracellular structures that may play a role in shaping the lupus autoantibody repertoire 蛋白组合是最近被描述的细胞内结构,可能在形成狼疮自身抗体库中发挥作用
1700 – B cells and autoantibodies Pub Date : 2021-11-01 DOI: 10.1136/lupus-2021-lupus21century.100
P. L. Carl, H. Fried, P. Cohen
{"title":"1705 Protein assemblages are newly described intracellular structures that may play a role in shaping the lupus autoantibody repertoire","authors":"P. L. Carl, H. Fried, P. Cohen","doi":"10.1136/lupus-2021-lupus21century.100","DOIUrl":"https://doi.org/10.1136/lupus-2021-lupus21century.100","url":null,"abstract":"1706 Figure 1 Abstracts A72 Lupus Science & Medicine 2021;8(Suppl 2):A1–A75 coright. on Jauary 6, 2022 by gest. P rocted by httpupus.bm jcom / Lpus S ci M d: frst pulished as 10.1136/lupu-lupus21century.101 on 4 N ovem er 221. D ow nladed fom Conclusions These data (Cui, et al. PLoS One 2018;13: e01931711), also show strong association of EBV with SLE with anti-EBNA1 being more frequent in SLE cases than in concurrent patient controls, supporting the known association of EBV infection with SLE. Further, anti-EBNA1 is virtually always present in SLE and is present more frequently in EBA-infected SLE patients than in EBV-infected controls, consistent with the hypothesis that anti-EBNA1 is the usual immune response foundation from which pathogenic SLE autoimmunity emerges. These results support a model of the etiology of SLE that begins with EBV infection, leading to anti-EBNA1 antibodies. Then, a subset of these heteroimmune anti-EBNA1 antibodies cross react with SLE autoantigens (e.g., Sm as in figure 1, (EBV image, courtesy of NIAID/NIH; SLE malar rash image, courtesy of Mayo Foundation, all rights reserved)) that then mature into an SLE autoantibody response and result in in life-threatening clinical SLE. The specific role of the other EBV gene products, EBNA2, EBNA3C, and EBNALP, in this process (figure 1) await elucidation. Acknowledgments Support is appreciated from US Department of Veterans Affairs Merit Award (I01 BX001834), and the National Institutes of Health (R01 AI24717 & U01 AI130830). 1707 ANTI-RNP ANTIBODIES ARE ASSOCIATED WITH THE INTERFERON GENE SIGNATURE BUT NOT COMPLEMENT ACTIVATION IN SLE Erika Hubbard*, David S Pisetsky, Peter Lipsky. AMPEL BioSolutions, LLC and RILITE Foundation, Charlottesville, VA, USA; Duke University Medical Center, Durham, NC, USA; VA Medical Center, Durham, NC, USA 10.1136/lupus-2021-lupus21century.102 Background Anti-nuclear antibodies are essential features of SLE and are important markers for both diagnosis and pathogenesis. Anti-double stranded DNA (dsDNA) antibodies, which are routinely monitored to assess disease activity, can form immune complexes that activate complement (C) and promote renal pathology. Relatively less is known about the roles of autoantibodies against RNA binding proteins (RBPs) in pathogenesis and about the relationship between antidsDNA, anti-RBPs, complement activation, and expression of the interferon (IFN) gene signature (IGS). Analysis of data from two clinical trials of tabalumab in SLE (Illuminate 1 & 2, GSE88884) was undertaken to understand these interrelationships. Methods Microarray data from 1620 active (SLEDAI 6), female SLE patients and accompanying laboratory measurements were analyzed. Gene set variation analysis (GSVA) determined enrichment of transcriptomic signatures in each patient. Linear regression analysis was used to determine relationships between IGS GSVA scores and C3 and/or C4 levels as well as autoantibody levels. Unbiased classification and regres","PeriodicalId":235290,"journal":{"name":"1700 – B cells and autoantibodies","volume":"36 6 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129688440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
1708 Preliminary data on the mapping of anti-mitochondrial antibodies in systemic lupus erythematosus 1708系统性红斑狼疮抗线粒体抗体图谱初步研究
1700 – B cells and autoantibodies Pub Date : 2021-11-01 DOI: 10.1136/lupus-2021-lupus21century.103
Y. Becker, E. Rollet-Labelle, Tania Lévesque, J. Leclerc, A. Julien, P. Fortin, É. Boilard
{"title":"1708 Preliminary data on the mapping of anti-mitochondrial antibodies in systemic lupus erythematosus","authors":"Y. Becker, E. Rollet-Labelle, Tania Lévesque, J. Leclerc, A. Julien, P. Fortin, É. Boilard","doi":"10.1136/lupus-2021-lupus21century.103","DOIUrl":"https://doi.org/10.1136/lupus-2021-lupus21century.103","url":null,"abstract":"","PeriodicalId":235290,"journal":{"name":"1700 – B cells and autoantibodies","volume":"9 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130009505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
1706 A model of lupus pathogenesis: anti-EBNA1 heteroantibodies initiate lupus by cross reacting with lupus autoantigens, resulting in lupus autoantibodies and clinical disease 1706狼疮发病机制模型:抗ebna1异源抗体通过与狼疮自身抗原交叉反应引发狼疮,导致狼疮自身抗体和狼疮临床疾病
1700 – B cells and autoantibodies Pub Date : 2021-11-01 DOI: 10.1136/lupus-2021-lupus21century.101
Viktoryia Laurynenka, Li-li Ding, L. Kottyan, M. Weirauch, K. Kaufman, J. James, J. Harley
{"title":"1706 A model of lupus pathogenesis: anti-EBNA1 heteroantibodies initiate lupus by cross reacting with lupus autoantigens, resulting in lupus autoantibodies and clinical disease","authors":"Viktoryia Laurynenka, Li-li Ding, L. Kottyan, M. Weirauch, K. Kaufman, J. James, J. Harley","doi":"10.1136/lupus-2021-lupus21century.101","DOIUrl":"https://doi.org/10.1136/lupus-2021-lupus21century.101","url":null,"abstract":"","PeriodicalId":235290,"journal":{"name":"1700 – B cells and autoantibodies","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116395471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
1702 Comparison of the B cell response to self- versus foreign- antigen in mice revealed by single cell transcriptomics 1702用单细胞转录组学研究小鼠B细胞对自体抗原和外源抗原反应的比较
1700 – B cells and autoantibodies Pub Date : 2021-11-01 DOI: 10.1136/lupus-2021-lupus21century.97
C. Castrillon, Léa Simoni, T. Broek, C. Poel, E. Akama‐Garren, M. Carroll
{"title":"1702 Comparison of the B cell response to self- versus foreign- antigen in mice revealed by single cell transcriptomics","authors":"C. Castrillon, Léa Simoni, T. Broek, C. Poel, E. Akama‐Garren, M. Carroll","doi":"10.1136/lupus-2021-lupus21century.97","DOIUrl":"https://doi.org/10.1136/lupus-2021-lupus21century.97","url":null,"abstract":"","PeriodicalId":235290,"journal":{"name":"1700 – B cells and autoantibodies","volume":"144 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132641271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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