Distinct dendritic cell subsets dictate the fate decision between effector and memory CD8+ T cell differentiation by a CD24-dependent mechanism

Taeg S. Kim; Stacey A. Gorski; Steven Hahn; Kenneth M. Murphy; Thomas J. Braciale

doi:10.1016/j.immuni.2014.02.004

Distinct dendritic cell subsets dictate the fate decision between effector and memory CD8⁺ T cell differentiation by a CD24-dependent mechanism

Taeg S. Kim, Stacey A. Gorski, Steven Hahn, Kenneth M. Murphy, Thomas J. Braciale

Research output: Contribution to journal › Article › peer-review

121 Scopus citations

Abstract

The contribution of different DC subsets to effector and memory CD8⁺ Tcell generation during infection and the mechanism by which DCs controls these fate decisions is unclear. Here we demonstrated that the CD103⁺ and CD11b^hi migratory respiratory DC (RDC) subsets after influenza virus infection activated naive virus-specific CD8⁺ Tcells differentially. CD103⁺ RDCs supported the generation of CD8⁺ T effector (Teff) cells, which migrate from lymph nodes to the infected lungs. In contrast, migrant CD11b^hi RDCs activated CD8⁺ Tcells characteristic of central memory CD8⁺ T (CD8⁺ Tcm) cells including retention within the draining lymph nodes. CD103⁺ RDCs expressed CD24 at an elevated level, contributing to the propensity of this DC subpopulation to support CD8⁺ Teff cell differentiation. Mechanistically, CD24 was shown to regulate CD8⁺ Tcell activation through HMGB1-mediated engagement of Tcell RAGE. Thus, there is distribution of labor among DC subsets in regulating CD8⁺ Tcell differentiation.

Original language	English
Pages (from-to)	400-413
Number of pages	14
Journal	Immunity
Volume	40
Issue number	3
DOIs	https://doi.org/10.1016/j.immuni.2014.02.004
State	Published - Mar 20 2014

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title = "Distinct dendritic cell subsets dictate the fate decision between effector and memory CD8+ T cell differentiation by a CD24-dependent mechanism",

abstract = "The contribution of different DC subsets to effector and memory CD8+ Tcell generation during infection and the mechanism by which DCs controls these fate decisions is unclear. Here we demonstrated that the CD103+ and CD11bhi migratory respiratory DC (RDC) subsets after influenza virus infection activated naive virus-specific CD8+ Tcells differentially. CD103+ RDCs supported the generation of CD8+ T effector (Teff) cells, which migrate from lymph nodes to the infected lungs. In contrast, migrant CD11bhi RDCs activated CD8+ Tcells characteristic of central memory CD8+ T (CD8+ Tcm) cells including retention within the draining lymph nodes. CD103+ RDCs expressed CD24 at an elevated level, contributing to the propensity of this DC subpopulation to support CD8+ Teff cell differentiation. Mechanistically, CD24 was shown to regulate CD8+ Tcell activation through HMGB1-mediated engagement of Tcell RAGE. Thus, there is distribution of labor among DC subsets in regulating CD8+ Tcell differentiation.",

author = "Kim, {Taeg S.} and Gorski, {Stacey A.} and Steven Hahn and Murphy, {Kenneth M.} and Braciale, {Thomas J.}",

note = "Funding Information: We thank B. Small for excellent technical assistance and members of the T.J.B. laboratory for insightful comments and helpful discussions. We also would like to thank V. Engelhard, T. Bender, and V. Laubach (University of Virginia, VA) for reagents and technical advice. This study is supported by the National Institutes of Health (R01 AI-15608, U19 AI-83024, and R01 HL-33391 to T.J.B.). ",

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AU - Gorski, Stacey A.

AU - Hahn, Steven

AU - Murphy, Kenneth M.

AU - Braciale, Thomas J.

N1 - Funding Information: We thank B. Small for excellent technical assistance and members of the T.J.B. laboratory for insightful comments and helpful discussions. We also would like to thank V. Engelhard, T. Bender, and V. Laubach (University of Virginia, VA) for reagents and technical advice. This study is supported by the National Institutes of Health (R01 AI-15608, U19 AI-83024, and R01 HL-33391 to T.J.B.).

PY - 2014/3/20

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N2 - The contribution of different DC subsets to effector and memory CD8+ Tcell generation during infection and the mechanism by which DCs controls these fate decisions is unclear. Here we demonstrated that the CD103+ and CD11bhi migratory respiratory DC (RDC) subsets after influenza virus infection activated naive virus-specific CD8+ Tcells differentially. CD103+ RDCs supported the generation of CD8+ T effector (Teff) cells, which migrate from lymph nodes to the infected lungs. In contrast, migrant CD11bhi RDCs activated CD8+ Tcells characteristic of central memory CD8+ T (CD8+ Tcm) cells including retention within the draining lymph nodes. CD103+ RDCs expressed CD24 at an elevated level, contributing to the propensity of this DC subpopulation to support CD8+ Teff cell differentiation. Mechanistically, CD24 was shown to regulate CD8+ Tcell activation through HMGB1-mediated engagement of Tcell RAGE. Thus, there is distribution of labor among DC subsets in regulating CD8+ Tcell differentiation.

AB - The contribution of different DC subsets to effector and memory CD8+ Tcell generation during infection and the mechanism by which DCs controls these fate decisions is unclear. Here we demonstrated that the CD103+ and CD11bhi migratory respiratory DC (RDC) subsets after influenza virus infection activated naive virus-specific CD8+ Tcells differentially. CD103+ RDCs supported the generation of CD8+ T effector (Teff) cells, which migrate from lymph nodes to the infected lungs. In contrast, migrant CD11bhi RDCs activated CD8+ Tcells characteristic of central memory CD8+ T (CD8+ Tcm) cells including retention within the draining lymph nodes. CD103+ RDCs expressed CD24 at an elevated level, contributing to the propensity of this DC subpopulation to support CD8+ Teff cell differentiation. Mechanistically, CD24 was shown to regulate CD8+ Tcell activation through HMGB1-mediated engagement of Tcell RAGE. Thus, there is distribution of labor among DC subsets in regulating CD8+ Tcell differentiation.

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Distinct dendritic cell subsets dictate the fate decision between effector and memory CD8⁺ T cell differentiation by a CD24-dependent mechanism

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