BCL-6 regulates chemokine gene transcription in macrophages

被引：138

作者：

Toney, LM

Cattoretti, G

Graf, JA

Merghoub, T

Pandolfi, PP

Dalla-Favera, R

Ye, BH

Dent, AL ^{[1
]}

机构：

[1] Indiana Univ, Sch Med, Dept Microbiol & Immunol, Indianapolis, IN 46202 USA

[2] Indiana Univ, Sch Med, Walther Oncol Ctr, Indianapolis, IN 46202 USA

[3] Walther Oncol Ctr, Indianapolis, IN 46208 USA

[4] Columbia Univ Coll Phys & Surg, Inst Canc Genet, New York, NY 10032 USA

[5] Columbia Univ Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA

[6] Cornell Univ, Grad Sch Med Sci, Mem Sloan Kettering Canc Ctr, Sloan Kettering Div,Dept Human Genet, New York, NY 10021 USA

[7] Cornell Univ, Grad Sch Med Sci, Mem Sloan Kettering Canc Ctr, Sloan Kettering Div,Mol Biol Program, New York, NY 10021 USA

[8] Albert Einstein Coll Med, Dept Cell Biol, Bronx, NY 10461 USA

[9] Albert Einstein Coll Med, Ctr Comprehens Canc, Bronx, NY 10461 USA

来源：

NATURE IMMUNOLOGY | 2000年 / 1卷 / 03期

关键词：

D O I：

10.1038/79749

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The transcriptional repressor protein BCL-6, implicated in the pathogenesis of B cell lymphoma, regulates lymphocyte differentiation and inflammation. We investigated the mechanism for the T helper cell subset 2 (T(H)2)-type inflammation that occurs in BCL-6(-/-) mice. Using chimeric mice we found that the T(H)2-type inflammation is dependent upon nonlymphoid cells. We identified three chemokines, MCP-1, MCP-3 and MRP-1,which are negatively regulated by BCL-6 in macrophages. Promoter analysis revealed that BCL-6 is a potent repressor of MCP-1 transcription. Our results provide a mechanism for the regulation of T(H)2-type inflammation by BCL-6 and link TH2 differentiation to innate immunity.

引用

页码：214 / 220

页数：7

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