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Jacobson, B.

Publications and source records attributed to Jacobson, B..

2 recordsLinked to original sources

IgE occupancy and antigen valency cooperate to control FcϵRI aggregation geometry and signaling efficiency

The crosslinking of IgE-bound Fc{varepsilon}RI by multivalent allergens initiates mast cell and basophil signaling underlying Type 1 allergy. Yet, how allergen properties and IgE occupancy impact receptor aggregation and downstream signaling remain unclear. We used Phl p 1-specific IgE and recombinant fusion proteins presenting a Phl p 1-derived peptide in defined valencies and positions (MB1N, MB2N, MB4N, MB1N1C) to probe antigen-dependent signaling. Tetravalent MB4N evoked stronger degranulation and Ca2+ response than bivalent antigens, MB2N and MB1N1C. MB4N was also capable of signaling at low IgE occupancy and in Lyn-deficient cells. Monte Carlo simulations predicted that MB4N forms larger, complex receptor aggregates, while MB2N and MB1N1C produce dimers and linear chains. Consistently, addition of MB4N showed larger aggregates by electron microscopy and slower mobility by single particle tracking, compared to bivalent antigens. Thus, allergen valency and epitope spatial arrangement dictate Fc{varepsilon}RI aggregate organization and subsequent effector cell activation.

immunology↗

PID-controller enhanced artificial beta-cells

Conventional management of diabetes via injection or external insulin pumps suffers from inconvenience and inability to accurately maintain blood glucose levels. A potential solution to these problems consists of implanting synthetic artificial {beta}-cells that can sense glucose and transcribe insulin protein. We focus on one such artificial {beta}-cell recently described in the work of Xie et al. Experimental results show these cells are able to release insulin and somewhat improve postprandial glucose levels in diabetic mice. However, they fail to achieve the degree of glucose regulation as in healthy mice. In our analysis, we explain that this artificial {beta}-cell system has a major disadvantage: it is a high-dimensional dynamic system but with little tuning space. Here, we propose a PID-controller-based enhanced artificial {beta}-cell design to solve this issue. Our results based on an analytical model and numerical simulations show that the computational method of PID-control can enhance engineered artificial {beta}-cells, such that they could perform better in regulating glucose levels in Type 1 diabetic mice compared with artificial {beta}-cells without PID-control: they could shut down the production of insulin in time and maintain a proper glycemia level, and there is more tuning space for artificial {beta}-cells with PID control.

systems biology↗