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B Cell Activation and Differentiation

B Cell Activation and Differentiation

The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...

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A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

Examining B-cell dynamics and responsiveness in different inflammatory milieus using an agent-based model.

Bryan Shin¹, Gary An¹, R Chase Cockrell¹

¹Department of Surgery, University of Vermont Larner College of Medicine, Burlington, Vermont, United States of America.

Plos Computational Biology

|January 23, 2024

Summary

Modeling B-cell dynamics reveals that chronic inflammation, such as from diabetes or obesity, impairs immune responses. This dysfunction affects B-cell immunity, increasing susceptibility to infections and impacting recovery, particularly in conditions like COVID-19.

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Flow Cytometric Characterization of Murine B Cell Development

Flow Cytometric Characterization of Murine B Cell Development

Published on: January 22, 2021

Area of Science:

Immunology
Computational Biology
Systems Biology

Background:

B-cells are crucial for immunity, producing antibodies and aiding in pathogen clearance.
Inflammatory conditions like sepsis, diabetes, obesity, and advanced age compromise B-cell function.
Dysfunctional B-cells, influenced by Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α), increase infection risk.

Purpose of the Study:

To model B-cell dynamics and investigate their response to varying systemic inflammation levels.
To understand how chronic inflammation impacts B-cell immunity and immune memory formation.

Main Methods:

Developed the B-cell Immunity Agent-based Model (BCIABM) incorporating B-cell subtypes, differentiation, and cytokines.
Calibrated the BCIABM to simulate responses to mild (immune memory) and severe (sepsis) antigen challenges.
Simulated B-cell responses under chronic low-level inflammation (simulating diabetes, obesity, advanced age) and validated against COVID-19 patient data.

Main Results:

The BCIABM accurately reproduced immune memory development and sepsis-induced immunoparalysis.
Simulations showed significantly reduced B-cell responsiveness with increasing chronic inflammation.
Model results aligned with observed COVID-19 infection data in a patient cohort with comorbidities.

Conclusions:

The BCIABM effectively models B-cell dynamics and immune responses across diverse inflammatory states.
Results support a conserved mechanism where chronic inflammation negatively correlates with B-cell responsiveness.
This model elucidates B-cell dysfunction in various conditions, explaining altered immune presentations.