Analyses of :
🧪B cell antibody persistence following hepatitis A and B and HPV immunisation revealed patterns of longevity and heterogeneity within and between responses, implying that this process is fine-tuned near a critical “flat” state between two dynamic regimes.
This critical state reflects the tuning of rates of the underlying regulatory network and is highly sensitive to variation in parameters, which amplifies lifespan differences between cells.
Current models for plasma cell lifespan are based on competition for space, or the proposition that lifespan is imprinted on plasma cells during the initial immune response.
In the first model,
1. 🧪new plasma cells may displace old plasma cells from the niche, a behaviour consistent with the crucial role of niche factors in plasma cell survival, as well as experiments
2. 🧪In this case, plasma cell lifespan reflects the balance between the carrying capacity of the niche and the arrival rate of new plasma cells and can therefore be in principle long.
The imprinted lifespan model, on the other hand, does not account for the possible role of competition in determining plasma cell lifespan. Moreover, it is unclear how the distribution of lifespans ranging from days to decades can be encoded by a biochemical network whose components are likely to have a lifespan of only hours to days, and how it can be set during B cell differentiation.
Fine-tuning can arise from the continuous influx of new plasma B cells and the ensuing competition among them for survival factors producing effective immune responses.
By operating near a critical state, the system is capable of generating both a population of short-lived plasma cells and a long-lasting population that can persist for decades.
Article Link Benjamin Simons et al: