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 Blood, 15 February 2008, Vol. 111, No. 4, pp. 1942-1945.
Prepublished online as a Blood First Edition Paper on November 30, 2007; DOI 10.1182/blood-2007-07-100750.

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HEMATOPOIESIS

Brief Report

The BXH2 mutation in IRF8 differentially impairs dendritic cell subset development in the mouse

Prafullakumar Tailor1, Tomohiko Tamura1, Herbert C. Morse, III2, and Keiko Ozato1

1 Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD; 2 Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD

Among dendritic cell (DC) subsets, CD8{alpha}+ DCs and plasmacytoid DCs (pDCs) produce high levels of IL12 and type I interferons (IFNs), respectively, and confer early innate immunity. Development of CD8{alpha}+ DCs and pDCs requires the interferon regulatory factor 8 (IRF8). Recently, a spontaneous point mutation was identified in the Irf8/Icsbp gene in the BXH2 mouse, which exhibits an immunodeficient phenotype similar to the IRF8 knockout (KO) mouse. We show that this mutation, designated IRF8R294C, abolishes the development of CD8{alpha}+ DCs without impairing pDC development, and eliminates production of IL12p40, while retaining that of type I IFNs. Electrophoretic mobility shift and chromatin immunoprecipitation assays indicated that IRF8R294C failed to interact with partner transcription factors and did not bind certain promoters that require partner interactions. Together, this work indicates that IRF8-partner interactions play different roles in CD8{alpha}+ DCs and pDCs, revealing a mechanistic separation that underlies development of these DC subsets.


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