GSBS Student Publications

Title

Role of apoptosis in the regulation of virus-induced T cell responses, immune suppression, and memory

UMMS Affiliation

Graduate School of Biomedical Sciences; Department of Pathology

Date

10-1-1995

Document Type

Article

Medical Subject Headings

Animals; Apoptosis; Cell Aging; Humans; *Immune Tolerance; *Immunologic Memory; Lymphocyte Activation; T-Lymphocytes; T-Lymphocytes, Cytotoxic; Virus Diseases

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

Apoptosis is an important mechanism enabling the selection of the non-self-reactive T cell repertoire and for maintaining homeostasis in the immune system after it has expanded to combat infections. Highly activated, proliferating T cells become susceptible to apoptosis driven by a number of stimuli, and T cells activated during a viral infection become susceptible to "activation induced cell death" after repeated stimulation through the T cell receptor (TcR). This is a major mechanism for the immune deficiencies observed during many viral infections. During infections with a high antigen load this can lead to a selective deletion of virus-specific cytotoxic T lymphocytes (CTL) and to the establishment of persistent infection. More commonly, the CTL control the infection first, and high levels of apoptosis in the expanded lymphocyte population occur after antigen and growth factors become limiting. This cell death does not seem to depend on TcR specificity, as the residual population contains a remarkably stable population of memory CTL precursors that approximate the frequency per CD8 cell of that seen during the peak of the acute infection. Subsequent infections with heterologous viruses result in an expansion and then an apoptotic elimination of T cells, with the consequence being a reduction in precursor CTL specific for the first virus. Thus, apoptosis shapes the quality and quantity of T cell memory.

Rights and Permissions

Citation: J Cell Biochem. 1995 Oct;59(2):135-42. Link to article on publisher's site

DOI of Published Version

10.1002/jcb.240590202

Related Resources

Link to Article in PubMed

Journal Title

Journal of cellular biochemistry

PubMed ID

8904307