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Published on: October 5, 2012
Role of bcl-2 and apoptosis in viral infections
A N Akbar1, M Salmon, G Janossy
1Department of Clinical Immunology, Royal Free Hospital School of Medicine, London, UK.
Insights
This review explores how apoptosis controls T cell populations during viral infections. It examines mechanisms that eliminate excess cells while retaining virus-specific T cells for future immunity.
Area of Science:
- Immunobiology
- Virology
- Cellular Biology
Background:
- Historically, research focused on lymphocyte proliferation to increase antigen-responsive cells.
- Current research investigates mechanisms controlling activated lymphocyte population size during viral infections.
Purpose of the Study:
- To review recent observations on the control of apoptosis in T cell populations during viral infections.
- To discuss how apoptosis co-exists with mechanisms for retaining fittest cells for future viral encounters.
Main Methods:
- Review of recent scientific literature on T cell apoptosis and viral infections.
- Analysis of mechanisms controlling T cell population size and retention.
Main Results:
- Apoptosis is a key physiological process for removing unwanted cells.
- Specific mechanisms ensure the retention of effective T cells post-infection.
Conclusions:
- Apoptosis plays a crucial role in regulating T cell numbers during viral infections.
- The interplay between apoptosis and cell retention mechanisms is vital for adaptive immunity.
Abstract:
For decades immunobiologists have focussed on lymphocyte activation leading to cellular proliferation as a means by which the numbers of antigen-responsive cells can be increased. The pendulum has now swung back and questions are being raised about the way in which the size of the activated lymphocyte populations, such as those found during certain acute viral infections, can be controlled. The process of apoptosis has gained widespread recognition as a physiological means by which unwanted cells can be removed. In this review we will discuss recent observations on the control of apoptosis in the activated and expanded T cell populations found during viral infections and how this process co-exists with certain mechanisms which enable the retention of the fittest cells which can participate in subsequent encounters with virus.
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