Extrafollicular IgD−CD27−CXCR5−CD11c− DN3 B cells infiltrate inflamed tissues in autoimmune fibrosis and in severe COVID-19
Summary: Although therapeutic B cell depletion dramatically resolves inflammation in many diseases in which antibodies appear not to play a central role, distinct extrafollicular pathogenic B cell subsets that accumulate in disease lesions have hitherto not been identified. The circulating immunoglo...
Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , |
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Format: | Article |
Language: | English |
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Elsevier
2023-06-01
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Series: | Cell Reports |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124723006411 |
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author | Hugues Allard-Chamard Naoki Kaneko Alice Bertocchi Na Sun Julie Boucau Hsiao-Hsuan Kuo Jocelyn R. Farmer Cory Perugino Vinay S. Mahajan Samuel J.H. Murphy Katherine Premo Thomas Diefenbach Musie Ghebremichael Grace Yuen Alekhya Kotta Zafer Akman Mathias Lichterfeld Bruce D. Walker Xu G. Yu Masafumi Moriyama Takashi Maehara Seiji Nakamura John H. Stone Robert F. Padera Shiv Pillai |
author_facet | Hugues Allard-Chamard Naoki Kaneko Alice Bertocchi Na Sun Julie Boucau Hsiao-Hsuan Kuo Jocelyn R. Farmer Cory Perugino Vinay S. Mahajan Samuel J.H. Murphy Katherine Premo Thomas Diefenbach Musie Ghebremichael Grace Yuen Alekhya Kotta Zafer Akman Mathias Lichterfeld Bruce D. Walker Xu G. Yu Masafumi Moriyama Takashi Maehara Seiji Nakamura John H. Stone Robert F. Padera Shiv Pillai |
author_sort | Hugues Allard-Chamard |
collection | DOAJ |
description | Summary: Although therapeutic B cell depletion dramatically resolves inflammation in many diseases in which antibodies appear not to play a central role, distinct extrafollicular pathogenic B cell subsets that accumulate in disease lesions have hitherto not been identified. The circulating immunoglobulin D (IgD)−CD27−CXCR5−CD11c+ DN2 B cell subset has been previously studied in some autoimmune diseases. A distinct IgD−CD27−CXCR5−CD11c− DN3 B cell subset accumulates in the blood both in IgG4-related disease, an autoimmune disease in which inflammation and fibrosis can be reversed by B cell depletion, and in severe COVID-19. These DN3 B cells prominently accumulate in the end organs of IgG4-related disease and in lung lesions in COVID-19, and double-negative B cells prominently cluster with CD4+ T cells in these lesions. Extrafollicular DN3 B cells may participate in tissue inflammation and fibrosis in autoimmune fibrotic diseases, as well as in COVID-19. |
first_indexed | 2024-03-13T06:20:13Z |
format | Article |
id | doaj.art-f6449a71ead94ed7a5350e782a784b4a |
institution | Directory Open Access Journal |
issn | 2211-1247 |
language | English |
last_indexed | 2024-03-13T06:20:13Z |
publishDate | 2023-06-01 |
publisher | Elsevier |
record_format | Article |
series | Cell Reports |
spelling | doaj.art-f6449a71ead94ed7a5350e782a784b4a2023-06-10T04:27:22ZengElsevierCell Reports2211-12472023-06-01426112630Extrafollicular IgD−CD27−CXCR5−CD11c− DN3 B cells infiltrate inflamed tissues in autoimmune fibrosis and in severe COVID-19Hugues Allard-Chamard0Naoki Kaneko1Alice Bertocchi2Na Sun3Julie Boucau4Hsiao-Hsuan Kuo5Jocelyn R. Farmer6Cory Perugino7Vinay S. Mahajan8Samuel J.H. Murphy9Katherine Premo10Thomas Diefenbach11Musie Ghebremichael12Grace Yuen13Alekhya Kotta14Zafer Akman15Mathias Lichterfeld16Bruce D. Walker17Xu G. Yu18Masafumi Moriyama19Takashi Maehara20Seiji Nakamura21John H. Stone22Robert F. Padera23Shiv Pillai24Ragon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA; Division of Rheumatology, Faculté de médecine et des sciences de la santé de l'Université de Sherbrooke et Centre de Recherche Clinique Étienne-Le Bel, Sherbrooke, QC J1K 2R1, CanadaRagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA; Section of Oral and Maxillofacial Oncology, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Fukuoka, JapanRagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA; Division of Rheumatology Allergy and Immunology, Massachusetts General Hospital, Boston, MA 02114, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA; Department of Pathology, Brigham and Women’s Hospital, Boston, MA 02115, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA; Department of Medicine, Brigham and Women’s Hospital, Boston, MA 02115, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA; Department of Biology and Institute of Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02139, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USASection of Oral and Maxillofacial Oncology, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Fukuoka, JapanRagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA; Section of Oral and Maxillofacial Oncology, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Fukuoka, JapanSection of Oral and Maxillofacial Oncology, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Fukuoka, JapanDivision of Rheumatology Allergy and Immunology, Massachusetts General Hospital, Boston, MA 02114, USADepartment of Pathology, Brigham and Women’s Hospital, Boston, MA 02115, USARagon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA; Corresponding authorSummary: Although therapeutic B cell depletion dramatically resolves inflammation in many diseases in which antibodies appear not to play a central role, distinct extrafollicular pathogenic B cell subsets that accumulate in disease lesions have hitherto not been identified. The circulating immunoglobulin D (IgD)−CD27−CXCR5−CD11c+ DN2 B cell subset has been previously studied in some autoimmune diseases. A distinct IgD−CD27−CXCR5−CD11c− DN3 B cell subset accumulates in the blood both in IgG4-related disease, an autoimmune disease in which inflammation and fibrosis can be reversed by B cell depletion, and in severe COVID-19. These DN3 B cells prominently accumulate in the end organs of IgG4-related disease and in lung lesions in COVID-19, and double-negative B cells prominently cluster with CD4+ T cells in these lesions. Extrafollicular DN3 B cells may participate in tissue inflammation and fibrosis in autoimmune fibrotic diseases, as well as in COVID-19.http://www.sciencedirect.com/science/article/pii/S2211124723006411CP: Immunology |
spellingShingle | Hugues Allard-Chamard Naoki Kaneko Alice Bertocchi Na Sun Julie Boucau Hsiao-Hsuan Kuo Jocelyn R. Farmer Cory Perugino Vinay S. Mahajan Samuel J.H. Murphy Katherine Premo Thomas Diefenbach Musie Ghebremichael Grace Yuen Alekhya Kotta Zafer Akman Mathias Lichterfeld Bruce D. Walker Xu G. Yu Masafumi Moriyama Takashi Maehara Seiji Nakamura John H. Stone Robert F. Padera Shiv Pillai Extrafollicular IgD−CD27−CXCR5−CD11c− DN3 B cells infiltrate inflamed tissues in autoimmune fibrosis and in severe COVID-19 Cell Reports CP: Immunology |
title | Extrafollicular IgD−CD27−CXCR5−CD11c− DN3 B cells infiltrate inflamed tissues in autoimmune fibrosis and in severe COVID-19 |
title_full | Extrafollicular IgD−CD27−CXCR5−CD11c− DN3 B cells infiltrate inflamed tissues in autoimmune fibrosis and in severe COVID-19 |
title_fullStr | Extrafollicular IgD−CD27−CXCR5−CD11c− DN3 B cells infiltrate inflamed tissues in autoimmune fibrosis and in severe COVID-19 |
title_full_unstemmed | Extrafollicular IgD−CD27−CXCR5−CD11c− DN3 B cells infiltrate inflamed tissues in autoimmune fibrosis and in severe COVID-19 |
title_short | Extrafollicular IgD−CD27−CXCR5−CD11c− DN3 B cells infiltrate inflamed tissues in autoimmune fibrosis and in severe COVID-19 |
title_sort | extrafollicular igd cd27 cxcr5 cd11c dn3 b cells infiltrate inflamed tissues in autoimmune fibrosis and in severe covid 19 |
topic | CP: Immunology |
url | http://www.sciencedirect.com/science/article/pii/S2211124723006411 |
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