Characterization of human DNGR-1+ BDCA3+ leukocytes as putative equivalents of mouse CD8alpha+ dendritic cells.
Characterization of human DNGR-1+ BDCA3+ leukocytes as putative equivalents of mouse CD8alpha+ dendritic cells.
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DOI:
10.1084/jem.20092618
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发表时间:
2010-06-07
期刊:
影响因子:
--
通讯作者:
Reis e Sousa C
中科院分区:
文献类型:
--
作者:
Poulin LF;Salio M;Griessinger E;Anjos-Afonso F;Craciun L;Chen JL;Keller AM;Joffre O;Zelenay S;Nye E;Le Moine A;Faure F;Donckier V;Sancho D;Cerundolo V;Bonnet D;Reis e Sousa C
In mouse, a subset of dendritic cells (DCs) known as CD8α+ DCs has emerged as an important player in the regulation of T cell responses and a promising target in vaccination strategies. However, translation into clinical protocols has been hampered by the failure to identify CD8α+ DCs in humans. Here, we characterize a population of human DCs that expresses DNGR-1 (CLEC9A) and high levels of BDCA3 and resembles mouse CD8α+ DCs in phenotype and function. We describe the presence of such cells in the spleens of humans and humanized mice and report on a protocol to generate them in vitro. Like mouse CD8α+ DCs, human DNGR-1+ BDCA3hi DCs express Necl2, CD207, BATF3, IRF8, and TLR3, but not CD11b, IRF4, TLR7, or (unlike CD8α+ DCs) TLR9. DNGR-1+ BDCA3hi DCs respond to poly I:C and agonists of TLR8, but not of TLR7, and produce interleukin (IL)-12 when given innate and T cell–derived signals. Notably, DNGR-1+ BDCA3+ DCs from in vitro cultures efficiently internalize material from dead cells and can cross-present exogenous antigens to CD8+ T cells upon treatment with poly I:C. The characterization of human DNGR-1+ BDCA3hi DCs and the ability to grow them in vitro opens the door for exploiting this subset in immunotherapy.
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DOI:
10.1084/jem.20071966
发表时间:
2007-12-24
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Bursch LS;Wang L;Igyarto B;Kissenpfennig A;Malissen B;Kaplan DH;Hogquist KA
通讯作者:
Hogquist KA
影响因子:
4.6
作者:
Ban, Y. -L.;Kong, B. -H.;Ma, Y. -Y.
通讯作者:
Ma, Y. -Y.
影响因子:
30.5
作者:
Bedoui, Sammy;Whitney, Paul G.;Heath, William R.
通讯作者:
Heath, William R.
影响因子:
4.4
作者:
Dzionek, A;Fuchs, A;Schmitz, J
通讯作者:
Schmitz, J
影响因子:
20.3
作者:
Caminschi, Irina;Proietto, Anna I.;Lahoud, Mireille H.
通讯作者:
Lahoud, Mireille H.