| Autor: |
Allard-Chamard, Hugues, Kaneko, Naoki, Bertocchi, Alice, Sun, Na, Boucau, Julie, Kuo, Hsiao-Hsuan, Farmer, Jocelyn R., Perugino, Cory, Mahajan, Vinay S., Murphy, Samuel J.H., Premo, Katherine, Diefenbach, Thomas, Ghebremichael, Musie, Yuen, Grace, Kotta, Alekhya, Akman, Zafer, Lichterfeld, Mathias, Walker, Bruce D., Yu, Xu G., Moriyama, Masafumi, Maehara, Takashi, Nakamura, Seiji, Stone, John H., Padera, Robert F., Pillai, Shiv |
| Zdroj: |
Cell Reports; June 2023, Vol. 42 Issue: 6 |
| Abstrakt: |
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. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
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