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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
CD70-driven chronic immune activation is protective against atherosclerosis
Ronald W van Olffen1, Alex M de Bruin, Mariska Vos
1Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Journal of Innate Immunity
|May 28, 2010
Summary
Sterile inflammation, driven by enhanced costimulation, unexpectedly protected against atherosclerosis in mice. This protection was linked to increased, but more apoptosis-prone, inflammatory monocytes.
Area of Science:
- Immunology
- Cardiovascular Research
- Innate Immunity
Background:
- Chronic infection and inflammation are linked to atherosclerosis development.
- The role of sterile inflammation (without infection) in atherosclerosis is less understood.
- Costimulatory signals play a role in immune responses and potentially atherosclerosis.
Purpose of the Study:
- To investigate if sterile chronic inflammation predisposes to atherosclerosis.
- To examine the impact of enhanced T cell costimulation (CD70 overexpression) on atherosclerosis.
- To understand the role of monocytes in inflammation-driven atherosclerosis.
Main Methods:
- Utilized a mouse model with CD70-transgenic (CD70TG) B cells on an ApoE*3-Leiden background.
- Analyzed atherosclerotic lesion development, serum cholesterol, and antibody levels.
- Characterized circulating monocyte populations, including activation, numbers, phagocytosis, TNFalpha production, and apoptosis.
Main Results:
- CD70TG mice showed strong protection against atherosclerotic lesion induction.
- Despite pro-inflammatory conditions (increased IFN gamma, activated Ly6C(+) monocytes), atherosclerosis was reduced.
- Monocytes from CD70TG mice were more prone to apoptosis, dependent on IFN gamma.
Conclusions:
- Sterile pro-inflammatory conditions can be protective against atherosclerosis.
- Reduced viability of circulating monocytes may underlie this protective effect.
- This highlights an unexpected role for costimulatory signals in innate immunity and atherosclerosis.
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