dorsal/arxiv
View SchemaMechanisms of B cell Synapse Formation Predicted by Stochastic Simulation
| Authors | Philippos K. Tsourkas, Nicole Baumgarth, Scott I. Simon, Subhadip Raychaudhuri |
|---|---|
| Categories | |
| ArXiv ID | q-bio/0609026 |
| URL | https://arxiv.org/abs/q-bio/0609026 |
| DOI | 10.1529/biophysj.106.094995 |
Abstract
The clustering of B cell receptor (BCR) molecules and the formation of the protein segregation structure known as the immunological synapse appears to precede antigen (Ag) uptake by B cells. The mature B cell synapse is characterized by a central cluster of BCR/Ag molecular complexes surrounded by a ring of LFA-1/ICAM-1 complexes. Recent experimental evidence shows receptor clustering in B cells can occur via mechanical or signaling-driven processes. An alternative mechanism of diffusion and affinity-dependent binding has been proposed to explain synapse formation in the absence of signaling-driven processes. In this work, we investigated the biophysical mechanisms that drive immunological synapse formation in B cells across the physiological range of BCR affinity (KA~10^6-10^10 M-1) through computational modeling. Our computational approach is based on stochastic simulation of diffusion and reaction events with a clearly defined mapping between probabilistic parameters of our model and their physical equivalents. We show that a diffusion-and-binding mechanism is sufficient to drive synapse formation only at low BCR affinity and for a relatively stiff B cell membrane that undergoes little deformation. We thus predict the need for alternative mechanisms: a difference in the mechanical properties of BCR/Ag and LFA-1/ICAM-1 bonds and/or signaling driven processes.
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"abstract": "The clustering of B cell receptor (BCR) molecules and the formation of the\nprotein segregation structure known as the immunological synapse appears to\nprecede antigen (Ag) uptake by B cells. The mature B cell synapse is\ncharacterized by a central cluster of BCR/Ag molecular complexes surrounded by\na ring of LFA-1/ICAM-1 complexes. Recent experimental evidence shows receptor\nclustering in B cells can occur via mechanical or signaling-driven processes.\nAn alternative mechanism of diffusion and affinity-dependent binding has been\nproposed to explain synapse formation in the absence of signaling-driven\nprocesses. In this work, we investigated the biophysical mechanisms that drive\nimmunological synapse formation in B cells across the physiological range of\nBCR affinity (KA~10^6-10^10 M-1) through computational modeling. Our\ncomputational approach is based on stochastic simulation of diffusion and\nreaction events with a clearly defined mapping between probabilistic parameters\nof our model and their physical equivalents. We show that a\ndiffusion-and-binding mechanism is sufficient to drive synapse formation only\nat low BCR affinity and for a relatively stiff B cell membrane that undergoes\nlittle deformation. We thus predict the need for alternative mechanisms: a\ndifference in the mechanical properties of BCR/Ag and LFA-1/ICAM-1 bonds and/or\nsignaling driven processes.",
"arxiv_id": "q-bio/0609026",
"authors": [
"Philippos K. Tsourkas",
"Nicole Baumgarth",
"Scott I. Simon",
"Subhadip Raychaudhuri"
],
"categories": [
"q-bio.QM",
"q-bio.SC"
],
"doi": "10.1529/biophysj.106.094995",
"title": "Mechanisms of B cell Synapse Formation Predicted by Stochastic Simulation",
"url": "https://arxiv.org/abs/q-bio/0609026"
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