CXCR3 ameliorates neutrophil-dependent disease severity in SARS-CoV-2 infection by regulating CD4+ T cell recruitment - Takeaways - MDSpire

CXCR3 ameliorates neutrophil-dependent disease severity in SARS-CoV-2 infection by regulating CD4+ T cell recruitment

  • By

  • Md Jashim Uddin

  • Claire Fleming

  • Nick R. Natale

  • Duncan Hart

  • Brett Moreau

  • Anthony Day

  • Judith Allen

  • William A. Petri

  • June 11, 2026

  • 0 min

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  • 1

    CXCR3 signaling is crucial for recruiting immune cells and mitigating neutrophil-driven pathology in SARS-CoV-2 infection.

  • 2

    Blocking CXCR3 resulted in worsened disease outcomes due to increased neutrophil infiltration and reduced T cell recruitment.

  • 3

    Mice with milder disease exhibited higher levels of CXCR3+ T cells, innate lymphoid cells, and macrophages in bronchoalveolar lavage fluid.

  • 4

    Depletion of neutrophils in CXCR3-blocked mice alleviated disease severity, highlighting the detrimental role of neutrophils.

  • 5

    Adoptive transfer of CXCR3+ CD4+ T cells conferred protection in RAG2-/- mice, emphasizing the importance of adaptive immunity.

Original Source(s)

CXCR3 ameliorates neutrophil-dependent disease severity in SARS-CoV-2 infection by regulating CD4+ T cell recruitment

  • by Md Jashim Uddin, Claire Fleming, Nick R. Natale, Duncan Hart, Brett Moreau, Anthony Day, Judith Allen, William A. Petri

  • June 11, 2026

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