A novel mutation in CD83 results in the development of a unique population of CD4+ T cells

被引:43
|
作者
García-Martínez, LF [1 ]
Appleby, MW [1 ]
Staehling-Hampton, K [1 ]
Andrews, DM [1 ]
Chen, YC [1 ]
McEuen, M [1 ]
Tang, P [1 ]
Rhinehart, RL [1 ]
Proll, S [1 ]
Paeper, B [1 ]
Brunkow, ME [1 ]
Grandea, AG [1 ]
Howard, ED [1 ]
Walker, DE [1 ]
Charmley, P [1 ]
Jonas, M [1 ]
Shaw, S [1 ]
Latham, JA [1 ]
Ramsdell, F [1 ]
机构
[1] Celltech Res & Dev Ltd, Bothell, WA 98021 USA
来源
JOURNAL OF IMMUNOLOGY | 2004年 / 173卷 / 05期
关键词
D O I
10.4049/jimmunol.173.5.2995
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Using a mouse mutagenesis screen, we have identified CD83 as being critical for the development of CD4(+) T cells and for their function postactivation. CD11c(+) dendritic cells develop and function normally in mice with a mutated CD83 gene but CD4(+) T cell development is substantially reduced. Additionally, we now show that those CD4(+) cells that develop in a CD83 mutant animal fail to respond normally following allogeneic stimulation. This is at least in part due to an altered cytokine expression pattern characterized by an increased production of IL-4 and IL-10 and diminished IL-2 production. Thus, in addition to its role in selection of CD4(+) T cells, absence of CD83 results in the generation of cells with an altered activation and cytokine profile.
引用
收藏
页码:2995 / 3001
页数:7
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