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PD-1highCXCR5-CD4+ peripheral helper T cells promote CXCR3+ plasmablasts in human acute viral infection.
Asashima, Hiromitsu; Mohanty, Subhasis; Comi, Michela; Ruff, William E; Hoehn, Kenneth B; Wong, Patrick; Klein, Jon; Lucas, Carolina; Cohen, Inessa; Coffey, Sarah; Lele, Nikhil; Greta, Leissa; Raddassi, Khadir; Chaudhary, Omkar; Unterman, Avraham; Emu, Brinda; Kleinstein, Steven H; Montgomery, Ruth R; Iwasaki, Akiko; Dela Cruz, Charles S; Kaminski, Naftali; Shaw, Albert C; Hafler, David A; Sumida, Tomokazu S.
  • Asashima H; Department of Neurology, Yale School of Medicine, New Haven, CT, USA; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Mohanty S; Section of Infectious Diseases, Department of Internal Medicine, Yale School of Medicine, Yale University, New Haven, CT, USA.
  • Comi M; Department of Neurology, Yale School of Medicine, New Haven, CT, USA; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Ruff WE; Department of Neurology, Yale School of Medicine, New Haven, CT, USA; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Hoehn KB; Department of Pathology, Yale School of Medicine, New Haven, CT, USA.
  • Wong P; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Klein J; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Lucas C; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Cohen I; Department of Neurology, Yale School of Medicine, New Haven, CT, USA; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Coffey S; Department of Neurology, Yale School of Medicine, New Haven, CT, USA; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Lele N; Department of Neurology, Yale School of Medicine, New Haven, CT, USA; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Greta L; Department of Neurology, Yale School of Medicine, New Haven, CT, USA; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Raddassi K; Department of Neurology, Yale School of Medicine, New Haven, CT, USA; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Chaudhary O; Section of Infectious Diseases, Department of Internal Medicine, Yale School of Medicine, Yale University, New Haven, CT, USA.
  • Unterman A; Section of Pulmonary, Critical Care and Sleep Medicine Section, Department of Internal Medicine, School of Medicine, Yale University, New Haven, CT, USA.
  • Emu B; Section of Infectious Diseases, Department of Internal Medicine, Yale School of Medicine, Yale University, New Haven, CT, USA.
  • Kleinstein SH; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA; Department of Pathology, Yale School of Medicine, New Haven, CT, USA; Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT, USA.
  • Montgomery RR; Department of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.
  • Iwasaki A; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA; Section of Infectious Diseases, Department of Internal Medicine, Yale School of Medicine, Yale University, New Haven, CT, USA; Howard Hughes Medical Institute, Chevy Chase, MD, USA.
  • Dela Cruz CS; Section of Pulmonary, Critical Care and Sleep Medicine Section, Department of Internal Medicine, School of Medicine, Yale University, New Haven, CT, USA.
  • Kaminski N; Section of Pulmonary, Critical Care and Sleep Medicine Section, Department of Internal Medicine, School of Medicine, Yale University, New Haven, CT, USA.
  • Shaw AC; Section of Infectious Diseases, Department of Internal Medicine, Yale School of Medicine, Yale University, New Haven, CT, USA.
  • Hafler DA; Department of Neurology, Yale School of Medicine, New Haven, CT, USA; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Sumida TS; Department of Neurology, Yale School of Medicine, New Haven, CT, USA. Electronic address: tomokazu.sumida@yale.edu.
Cell Rep ; 42(1): 111895, 2023 01 31.
Article in English | MEDLINE | ID: covidwho-2227691
ABSTRACT
T cell-B cell interaction is the key immune response to protect the host from severe viral infection. However, how T cells support B cells to exert protective humoral immunity in humans is not well understood. Here, we use COVID-19 as a model of acute viral infections and analyze CD4+ T cell subsets associated with plasmablast expansion and clinical outcome. Peripheral helper T cells (Tph cells; denoted as PD-1highCXCR5-CD4+ T cells) are significantly increased, as are plasmablasts. Tph cells exhibit "B cell help" signatures and induce plasmablast differentiation in vitro. Interestingly, expanded plasmablasts show increased CXCR3 expression, which is positively correlated with higher frequency of activated Tph cells and better clinical outcome. Mechanistically, Tph cells help B cell differentiation and produce more interferon γ (IFNγ), which induces CXCR3 expression on plasmablasts. These results elucidate a role for Tph cells in regulating protective B cell response during acute viral infection.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Programmed Cell Death 1 Receptor / COVID-19 Type of study: Prognostic study Limits: Humans Language: English Journal: Cell Rep Year: 2023 Document Type: Article Affiliation country: J.celrep.2022.111895

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Programmed Cell Death 1 Receptor / COVID-19 Type of study: Prognostic study Limits: Humans Language: English Journal: Cell Rep Year: 2023 Document Type: Article Affiliation country: J.celrep.2022.111895