AI Article Synopsis
- The activation of self-reactive CD8 T cells leads to a mechanism of peripheral tolerance characterized by the loss of CD8 marker expression.
- Research indicates that defects in Fas and FasL result in an accumulation of double-negative T cells, previously thought to stem from CD8 cells.
- The study found that Fas and FasL play a crucial role in maintaining CD8 expression during repeated antigen exposure and self-antigen interactions, highlighting their significance in regulating immune tolerance.
Article Abstract
Activation of self-reactive CD8 T cells induces a peripheral tolerance mechanism that involves loss of CD8 expression. Because genetic deficiency of and causes the accumulation of double-negative (DN; CD3 TCR-αβ CD4 CD8) T cells that have been proposed to derive from CD8 cells, we decided to explore the role of Fas and FasL in self-antigen-induced CD8 downregulation. To this end, we quantified Fas and FasL induction by different stimuli and analyzed the effects of Fas/FasL deficiency during a protective immune response and after exposure to self-antigens. Our data describes how Fas and FasL upregulation differs depending on the setting of CD8 T cell activation and demonstrates that Fas/FasL signaling maintains CD8 expression during repetitive antigen stimulation and following self-antigen encounter. Together, our results reveal an unexpected role of Fas/FasL signaling and offer a new insight into the role of these molecules in the regulation of immune tolerance.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8024570 | PMC |
| http://dx.doi.org/10.3389/fimmu.2021.635862 | DOI Listing |
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