CTLA-4 checkpoint signalling modulates germinal centre dynamics and antibody avidity during Borrelia burgdorferi infection in mice.

Blocking CTLA-4 during Borrelia burgdorferi infection in mice increases plasma cell numbers and significantly enhances the magnitude and avidity of Borrelia-specific IgG, including IgG2a.

• Why it matters: Murine Lyme borreliosis features low-avidity antibodies despite strong immunity, but the T-cell checkpoint mechanisms shaping germinal center selection and antibody quality are unclear.
• What they did: The study profiled draining lymph node cells by single-cell RNA sequencing at days 7 and 14, then treated infected mice with anti-CTLA-4 blocking antibody to test inhibitory signaling effects.
• The result: CTLA-4 blockade improved humoral control by boosting germinal center output and antibody quality, suggesting CTLA-4-dependent inhibitory signaling contributes to defective antibody responses during persistent infection.

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