Antibody Consumption-Driven Dynamic Competition: A Systems Hypothesis for the Transition from Acute Immune Response to Post-Infection Sequelae
The mechanisms underlying the formation of post-infection sequelae are complex and remain controversial. This hypothesis integrates Bystryn's antibody feedback phenomenon and Imbiakha's immune cost theory, proposing for the first time a "Consumption-Driven Dynamic Competition of Antibody Clones" mechanism. This mechanism posits that the immune system may regulate the proliferation and differentiation of corresponding B cell clones by sensing and responding to the consumption rate of specific antibodies. This competition, driven by differences in consumption rates, might not only influence pathogen clearance efficiency and associated acute pathology during the antigen growth phase but also critically mediate the onset, development, and even resolution of post-infection sequelae during the antigen decay and homeostasis re-establishment phases. The proposed three-phase "consumption-driven dynamic competition" model provides a unified and dynamic explanatory framework for understanding the significant individual variability and dynamic evolution of post-infection immune outcomes (including the emergence and self-limitation of acute symptoms, the formation and persistence of chronic sequelae, and symptom fluctuations or resolution). It emphasizes not just specific molecules but the macroscopic dynamics of competition and selection within the immune system, offering a theoretical basis for exploring new intervention strategies for sequelae (e.g., by regulating the balance of antibody competition).