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Dendritic cell subsets require cis-activation for cytotoxic CD8 T-cell induction

Author

Listed:
  • A Nicole Desch

    (National Jewish Health and UC Denver Anschutz Campus)

  • Sophie L. Gibbings

    (National Jewish Health)

  • Eric T. Clambey

    (UC Denver Anschutz Campus)

  • William J. Janssen

    (National Jewish Health)

  • Jill E. Slansky

    (National Jewish Health and UC Denver Anschutz Campus)

  • Ross M. Kedl

    (National Jewish Health and UC Denver Anschutz Campus)

  • Peter M. Henson

    (National Jewish Health and UC Denver Anschutz Campus
    National Jewish Health)

  • Claudia Jakubzick

    (National Jewish Health and UC Denver Anschutz Campus
    National Jewish Health)

Abstract

Dendritic cells (DCs) are required for the induction of cytotoxic T cells (CTL). In most tissues, including the lung, the resident DCs fall into two types expressing the integrin markers CD103 and CD11b. The current supposition is that DC function is predetermined by lineage, designating the CD103+ DC as the major cross-presenting DC able to induce CTL. Here we show that Poly I:C (TLR3 agonist) or R848 (TLR7 agonist) do not activate all endogenous DCs. CD11b+ DCs can orchestrate a CTL response in vivo in the presence of a TLR7 agonist but not a TLR3 agonist, whereas CD103+ DCs require ligation of TLR3 for this purpose. This selectivity does not extend to antigen cross-presentation for T-cell proliferation but is required for induction of cytotoxicity. Thus, we demonstrate that the ability of DCs to induce functional CTLs is specific to the nature of the pathogen-associated molecular pattern (PAMP) encountered by endogenous DC.

Suggested Citation

  • A Nicole Desch & Sophie L. Gibbings & Eric T. Clambey & William J. Janssen & Jill E. Slansky & Ross M. Kedl & Peter M. Henson & Claudia Jakubzick, 2014. "Dendritic cell subsets require cis-activation for cytotoxic CD8 T-cell induction," Nature Communications, Nature, vol. 5(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5674
    DOI: 10.1038/ncomms5674
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