Efficient presentation of soluble antigen by cultured human dendritic cells is maintained by granulocyte/macrophage colony-stimulating factor plus interleukin 4 and downregulated by tumor necrosis factor alpha.
Efficient presentation of soluble antigen by cultured human dendritic cells is maintained by granulocyte/macrophage colony-stimulating factor plus interleukin 4 and downregulated by tumor necrosis factor alpha.
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DOI:
10.1084/jem.179.4.1109
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发表时间:
1994-04-01
影响因子:
4.4
通讯作者:
Lanzavecchia, Antonio
中科院分区:
文献类型:
--
作者:
Sallusto, Federica;Lanzavecchia, Antonio
Using granulocyte/macrophage colony-stimulating factor (GM-CSF) and interleukin 4 we have established dendritic cell (DC) lines from blood mononuclear cells that maintain the antigen capturing and processing capacity characteristic of immature dendritic cells in vivo. These cells have typical dendritic morphology, express high levels of major histocompatibility complex (MHC) class I and class II molecules, CD1, Fc gamma RII, CD40, B7, CD44, and ICAM-1, and lack CD14. Cultured DCs are highly stimulatory in mixed leukocyte reaction (MLR) and are also capable of triggering cord blood naive T cells. Most strikingly, these DCs are as efficient as antigen-specific B cells in presenting tetanus toxoid (TT) to specific T cell clones. Their efficiency of antigen presentation can be further enhanced by specific antibodies via FcR- mediated antigen uptake. Incubation of these cultured DCs with tumor necrosis factor alpha (TNF-alpha) or soluble CD40 ligand (CD40L) for 24 h results in an increased surface expression of MHC class I and class II molecules, B7, and ICAM-1 and in the appearance of the CD44 exon 9 splice variant (CD44-v9); by contrast, Fc gamma RII is markedly and sometimes completely downregulated. The functional consequences of the short contact with TNF-alpha are in increased T cell stimulatory capacity in MLR, but a 10-fold decrease in presentation of soluble TT and a 100-fold decrease in presentation of TT-immunoglobulin G complexes.
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影响因子:
15.3
作者:
KOCH, F;HEUFLER, C;KAMPGEN, E;SCHNEEWEISS, D;BOCK, G;SCHULER, G
通讯作者:
SCHULER, G
影响因子:
5.4
作者:
DEBRUIJN, MLH;NIELAND, JD;MELIEF, CJM
通讯作者:
MELIEF, CJM
DOI:
10.1016/0167-5699(92)90198-g
发表时间:
1992-01-01
期刊:
IMMUNOLOGY TODAY
影响因子:
--
作者:
JANEWAY, CA
通讯作者:
JANEWAY, CA
DOI:
10.1073/pnas.90.7.3038
发表时间:
1993-04-01
影响因子:
11.1
作者:
INABA, K;INABA, M;STEINMAN, RM
通讯作者:
STEINMAN, RM
DOI:
10.1084/jem.177.2.397
发表时间:
1993-02-01
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Holt PG;Oliver J;Bilyk N;McMenamin C;McMenamin PG;Kraal G;Thepen T
通讯作者:
Thepen T