Critical roles of interferon regulatory factor 4 in CD11bhighCD8α- dendritic cell development

被引：256

作者：

Suzuki, S

Honma, K

Matsuyama, T

Suzuki, K

Toriyama, K

Akitoyo, I

Yamamoto, K

Suematsu, T

Nakamura, M

Yui, K

Kumatori, A

机构：

[1] Nagasaki Univ, Grad Sch Biomed Sci, Dept Mol Microbiol & Immunol, Nagasaki 8528523, Japan

[2] Nagasaki Univ, Grad Sch Biomed Sci, Dept Host Def Biochem, Nagasaki 8528523, Japan

[3] Nagasaki Univ, Grad Sch Biomed Sci, Dept Pathol, Nagasaki 8528523, Japan

[4] Nagasaki Univ, Grad Sch Biomed Sci, Inst Trop Med, Cent Lab, Nagasaki 8528523, Japan

[5] Nagasaki Univ, Grad Sch Biomed Sci, Dept Translat Med Sci, Div Immunol, Nagasaki 8528523, Japan

[6] Nagasaki Univ, Grad Sch Biomed Sci, Electron Microscope Ctr, Nagasaki 8528523, Japan

[7] Natl Inst Infect Dis, Lab Biodef, Shinjuku Ku, Tokyo 1628640, Japan

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2004年 / 101卷 / 24期

关键词：

D O I：

10.1073/pnas.0402139101

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

IFN regulatory factors (IRFs) are a family of transcription factors that play an essential role in the homeostasis and function of immune systems. Recent studies indicated that IRF-8 is critical for the development of CD11b(low)CD8alpha(+) conventional dendritic cells (DCs) and plasmacytoid DCs. Here we show that IRF-4 is important for CD11b(high)CD8alpha(-) conventional DCs. The development of CD11b(high) DCs from bone marrow of IRF-4(-/-) mice was severely impaired in two culture systems supplemented with either GM-CSF or Flt3-ligand. In the IRF-4(-/-) spleen, the number of CD4(+)CD8alpha(-) DCs, a major subset of CD11b(high) DCs, was severely reduced. IRF-4 and IRF-8 were expressed in the majority of CD11b(high) CD4(+)CD8alpha(-) DCs and CD11b(low)CD8alpha(+) DCs, respectively, in a mutually exclusive manner. These results imply that IRF-4 and IRF-8 selectively play critical roles in the development of the DC subsets that express them.

引用

页码：8981 / 8986

页数：6

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