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Blood, 15 November 2006, Vol. 108, No. 10, pp. 3253-3261.
Prepublished online as a Blood First Edition Paper on July 25, 2006; DOI 10.1182/blood-2006-06-027599.
 Previous Article | Next Article 
Submitted January 17, 2006
Accepted July 4, 2006
Type I interferons directly regulate lymphocyte
recirculation and cause transient blood lymphopenia
Elisabeth Kamphuis, Tobias Junt, Zoe Waibler, Reinhold Forster, and Ulrich Kalinke*
Paul-Ehrlich-Institut, Division of Immunology, Langen, Germany
CBR Institute for Biomedical Research & Department of Pathology, Harvard Medical School, MA, USA
Hannover Medical School, Institute of Immunology, Hannover, Germany
* Corresponding author; email: kalul{at}pei.de.
Early viral infection is often associated with
lymphopenia, a transient reduction of blood lymphocyte
counts long before onset of clinical symptoms. We have
investigated lymphopenia in mice infected with vesicular
stomatitis virus (VSV) or treated with the Toll-like
receptor (TLR) agonists poly(I:C) and R-848. In all
cases analyzed, lymphopenia was critically dependent on
type I interferon receptor (IFNAR) signaling. Using bone
marrow-chimeric mice, radio-resistant cells, such as
stroma and endothelium, could be excluded as type I
interferon (IFN- / ) targets for the
induction of lymphopenia. Instead, adoptive transfer
experiments and studies in conditionally gene-targeted
mice with a B or T cell-specific IFNAR deletion
demonstrated that IFN-/ exerted a direct
effect on lymphocytes that was necessary and largely
sufficient to induce lymphopenia. Furthermore, following
treatment with R-848 we found that other cytokines such
as TNF- also played a role in T cell
lymphopenia. Investigation of the molecular mechanism
revealed that lymphopenia was mainly independent of G
protein-coupled receptors (GPCRs) and chemokines. In an
adhesion assay, B cells of poly(I:C)-treated mice showed
moderately increased adhesion to ICAM-1, but not to VCAM-
1. In conclusion, our data identify a new effect of
direct IFN-/ stimulation of lymphocytes
that profoundly affects lymphocyte redistribution.
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