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| Format: | Recurso digital |
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Zenodo
2026
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| Online Access: | https://doi.org/10.5281/zenodo.18163641 |
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Table of Contents:
- <p>Adaptive biological systems must generate diversity while maintaining stability under finite<br>regulatory capacity. In adaptive immunity, this balance is achieved through oligoclonal competi-<br>tion within germinal centers, enabling selection while suppressing destructive interference. Here<br>we describe a distinct failure mode, termed oligoclonal capture, in which a small set of lineages<br>ceases to compete under governance and instead captures the regulatory machinery itself. This<br>transition suppresses comparative selection, disables exit mechanisms, and distorts signalling,<br>producing apparent stability with loss of recoverability. We argue that oligoclonal capture pro-<br>vides a unifying framework for understanding chronic immune dysfunction, autoimmune persis-<br>tence, and broader governance failures that generate systemic externalities. Importantly, this<br>perspective reframes pathology not as excessive activation or insufficient diversity, but as failure<br>of governance under capacity constraints.<br>Key Points<br>• Healthy adaptive systems rely on bounded oligoclonal competition, not monoclonality or<br>unstructured diversity.<br>• Oligoclonal capture occurs when dominant lineages control selection rather than being subject<br>to it.<br>• This failure mode produces stability without recoverability and is characterised by hysteresis.<br>• Memory records survival but does not confer legitimacy or indefinite persistence.<br>• The framework has implications for chronic immune disease, public health resilience, and<br>global governance.</p>