A Novel Mutation in CD83 Results in the Development of a Unique Population of CD4+ T Cells
Author(s) -
León F. Garcı́a-Martı́nez,
Mark W. Appleby,
Karen StaehlingHampton,
Dawn M. Andrews,
Yuching Chen,
Mark McEuen,
Phuong Tang,
Rebecca L. Rhinehart,
Sean Proll,
Bryan Paeper,
Mary E. Brunkow,
Andres G. Grandea,
Edward D. Howard,
D. Walker,
Patrick Charmley,
Mechthild Jonas,
Stevan Shaw,
John Latham,
Fred Ramsdell
Publication year - 2004
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.173.5.2995
Subject(s) - cd11c , biology , microbiology and biotechnology , mutant , cytokine , mutagenesis , population , mutation , t cell , function (biology) , immunology , phenotype , gene , immune system , genetics , medicine , environmental health
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.
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