期刊
NATURE IMMUNOLOGY
卷 22, 期 7, 页码 809-819出版社
NATURE PORTFOLIO
DOI: 10.1038/s41590-021-00949-7
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资金
- National Institutes of Health [T32GM007753]
CD8(+) T cells play critical roles in infection, cancer, and autoimmunity, but may exhibit dysfunction in different contexts. In cancer and chronic infections, CD8(+) T cells can become exhausted, while in autoimmunity, they retain the ability to cause host tissue damage.
Sharpe and colleagues review salient aspects of CD8(+) T cell dysfunction in cancer, chronic viral infections and autoimmunity, with a view of developing new ways to alleviate T cell exhaustion and enhance CD8(+) T cell functions in cancer and chronic viral infection, as well as strategies to induce or augment exhaustion-like features to treat autoimmunity. CD8(+) T cells are critical mediators of cytotoxic effector function in infection, cancer and autoimmunity. In cancer and chronic viral infection, CD8(+) T cells undergo a progressive loss of cytokine production and cytotoxicity, a state termed T cell exhaustion. In autoimmunity, autoreactive CD8(+) T cells retain the capacity to effectively mediate the destruction of host tissues. Although the clinical outcome differs in each context, CD8(+) T cells are chronically exposed to antigen in all three. These chronically stimulated CD8(+) T cells share some common phenotypic features, as well as transcriptional and epigenetic programming, across disease contexts. A better understanding of these CD8(+) T cell states may reveal novel strategies to augment clearance of chronic viral infection and cancer and to mitigate self-reactivity leading to tissue damage in autoimmunity.
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