Antibody feedback reshapes B cell selection during immune response

Researchers uncover a new mechanism governing how the immune system selects the most effective B cells, with implications for vaccine design.

Published on Feb. 14, 2026

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Researchers at the Ragon Institute, in collaboration with Scripps Research Institute, have revealed a surprising mechanism governing how the immune system selects the most effective B cells during an immune response. The study, published in Immunity, challenges the long-held belief that B cell selection is purely competitive, showing that B cells with the strongest binding affinity can actually suppress weaker-binding cells targeting the same site, creating a hyperlocal feedback loop regulated by the antibodies themselves. This discovery has significant implications for vaccine design, suggesting that a broader, more diverse antibody response may be more effective than a strong antibody response focused on the highest-affinity B cells.

Why it matters

This research challenges the traditional understanding of how the immune system selects B cells during an immune response, revealing a more nuanced process regulated by antibody feedback. This has important implications for vaccine design, as it suggests that vaccines should focus on eliciting a broader range of antibodies, not just the strongest-binding ones. This is particularly relevant for viruses like HIV and influenza, which are known for their ability to mutate and evade the immune system.

The details

The team found that B cells with the strongest binding affinity don't necessarily spend the most time refining their antibodies within germinal centers, the sites where B cells mature. Surprisingly, these high-affinity cells can actually suppress weaker-binding cells targeting the same site, creating a hyperlocal feedback loop regulated by the antibodies themselves. "Antibody binding only needs to be so high for protection. Eventually, you will get diminishing returns," explains Facundo Batista, PhD, principal investigator and co-corresponding author of the study. "Braking the further development of already effective binders redirects the germinal centers to other targets. Antibodies themselves are thus driving antibody diversity and a broader response."

  • The research was published in Immunity in February 2026.

The players

Facundo Batista

A professor of biology at MIT and associate director of the Ragon Institute, Batista has dedicated his career to understanding the intricacies of B cell biology. His research focuses on how, where, and when B cell responses develop, with the ultimate goal of improving vaccine and therapeutic strategies.

Ragon Institute

A collaborative research institute focused on understanding the immune system and developing new vaccines and therapies.

Scripps Research Institute

A non-profit research organization dedicated to advancing scientific knowledge and developing new treatments for human diseases.

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What they’re saying

“Antibody binding only needs to be so high for protection. Eventually, you will get diminishing returns.”

— Facundo Batista, Principal Investigator and Co-Corresponding Author (Immunity)

What’s next

Future studies will focus on confirming these findings in human subjects and exploring how individual variations in immune responses influence the effectiveness of this feedback mechanism. This could potentially lead to personalized immunization strategies tailored to an individual's unique immune profile.

The takeaway

This discovery challenges the long-held belief that B cell selection during an immune response is purely competitive, revealing a more nuanced process regulated by antibody feedback. This has significant implications for vaccine design, suggesting that a broader, more diverse antibody response may be more effective than a strong antibody response focused on the highest-affinity B cells.