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Study Offers First Insights into BCL-6 Regulation of Type 2 Inflammation

  September, 1 2000 2:47
your information resource in human molecular genetics
Repressor controls chemokines

Nature Immunology pages 214-220, News and Views page 189.

The BCL6 gene is implicated in B cell lymphomas, in which the regulation of many genes goes haywire.

But the protein BCL-6 doesn’t turn genes on that shouldn’t be on ­ it turns genes off. Mice that lack BCL-6 get an aggressive general inflammation that leads to death. Vital organs such as the spleen and liver are severely affected, and abnormal numbers of immune cells are present in these mice. The pattern of cells present ­ monocytes, eosinophils, type 2 helper T (TH2) cells, mast cells and B cells that produce the “allergy antibody” IgE ­ indicate that it is a type 2 inflammation.

How does the loss of one protein, BCL-6, lead to this state? In the September issue of Nature Immunology [Vol. 1, No. 3], researchers from Indiana University report the first insights into BCL-6 regulation of type 2 inflammation. The inflammation in BCL-6­deficient mice required cells such as macrophages, which produced a much greater amount of certain factors. Called chemokines, these factors attract the cell types typically found in type 2 inflammation.

The authors went on to show that the genes for three chemokines, MCP-1, MCP-3 and MRP-1, are repressed by BCL-6 in normal macrophages. In mice that lack BCL-6, the exuberant expression of these chemokines leads to severe TH2-type inflammation and eventual death of the mice.

A News & Views was written on this paper by Paul Rothman of Columbia University.

Contact Information:

Alexander L. Dent
Indiana University
School of Medicine
Department of Microbiology and Immunology
The Walther Oncology Center
Indianapolis, IN 46202
Tel: 317-274-7524
Fax: 317-274-7592
E-mail: adent2@iupui.edu

Paul Rothman
Columbia University
Dept of Microbiology and Medicine
630 W 168th St
New York, NY 10032
Tel: 212 305-1984
Fax: 212 305-1870
E-mail: pbr3@columbia.edu

(C) Nature Immunology, press release.

Message posted by: Trevor M. D'Souza

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