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Cytotoxic T-cell immunity to virus-infected non-haematopoietic cells requires presentation of exogenous antigen

Author

Listed:
  • Luis J. Sigal

    (University of Massachusetts Medical Center)

  • Shane Crotty

    (University of California)

  • Raul Andino

    (University of California)

  • Kenneth L. Rock

    (University of Massachusetts Medical Center)

Abstract

Cytotoxic T lymphocytes (CTLs) are thought to detect viral infections by monitoring the surface of all cells for the presence of viral peptides bound to major histocompatibility complex (MHC) class I molecules. In most cells, peptides presented by MHC class I molecules are derived exclusively from proteins synthesized by the antigen-bearing cells1. Macrophages and dendritic cells also have an alternative MHC class I pathway that can present peptides derived from extracellular antigens; however, the physiological role of this process is unclear2. Here we show that virally infected non-haematopoietic cells are unable to stimulate primary CTL-mediated immunity directly. Instead, bone-marrow-derived cells are required as antigen-presenting cells (APCs) to initiate anti-viral CTL responses. In these APCs, the alternative (exogenous) MHC class I pathway is the obligatory mechanism for the initiation of CTL responses to viruses that infect only non-haematopoietic cells.

Suggested Citation

  • Luis J. Sigal & Shane Crotty & Raul Andino & Kenneth L. Rock, 1999. "Cytotoxic T-cell immunity to virus-infected non-haematopoietic cells requires presentation of exogenous antigen," Nature, Nature, vol. 398(6722), pages 77-80, March.
    • Handle: RePEc:nat:nature:v:398:y:1999:i:6722:d:10.1038_18038
    DOI: 10.1038/18038
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    Cited by:

    1. Yan Wang & Quan Zhang & Tingting He & Yechen Wang & Tianqi Lu & Zengge Wang & Yiyi Wang & Shen Lin & Kang Yang & Xinming Wang & Jun Xie & Ying Zhou & Yazhen Hong & Wen-Hsien Liu & Kairui Mao & Shih-Ch, 2023. "The transcription factor Zeb1 controls homeostasis and function of type 1 conventional dendritic cells," Nature Communications, Nature, vol. 14(1), pages 1-20, December.

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