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Blood, 1 November 2006, Vol. 108, No. 9, pp. 3072-3078.
Prepublished online as a Blood First Edition Paper on May 25, 2006; DOI 10.1182/blood-2006-04-016923.
 Previous Article | Next Article 
Submitted April 13, 2006
Accepted May 8, 2006
Mucosal but not peripheral FOXP3+ regulatory T cells are
highly increased in untreated HIV infection and normalize
after suppressive HAART
Hans-Jorg Epple*, Christoph Loddenkemper, Desiree Kunkel, Hanno Troeger, Jochen Maul, Verena Moos, Erika Berg, Reiner Ullrich, Joerg-Dieter Schulzke, Harald Stein, Rainer Duchmann, Martin Zeitz, and Thomas Schneider
Charite - Universitaetsmedizin Berlin, Campus Benjamin Franklin, Med. Klinik I
Charite - Universitaetsmedizin Berlin, Campus Benjamin Franklin, Institute for Pathology
* Corresponding author; email: hans-joerg.epple{at}charite.de.
Recent evidence indicates that regulatory T cells (Treg)
play an important role in HIV infection. However,
although the gastrointestinal mucosa is a key
compartment in HIV disease, no data on mucosal Treg in
HIV infection are available. In this study, we compared
the frequency of Treg in duodenal mucosa and peripheral
blood (PB) of 11 treatment-naive and 9 suppressively
treated HIV-infected patients with those of 6 patients
with norovirus infection and 12 normal controls. Treg
were quantified by immunohistochemistry (CD3/FOXP3) and
further characterized (CD25, CTLA-4, GITR) by
immunohistochemistry, immunofluorescence and FACS.
Frequency as well as absolute count of mucosal Treg were
highly increased in untreated but normal in treated HIV
patients. In contrast in PB of HIV patients, the
absolute number of Treg was not increased and their
frequency was only slightly elevated. In norovirus
infection, frequency of mucosal Treg in the CD4+ T cell
subset was not elevated. The high increase in count and
frequency of mucosal Treg seems to be a characteristic
feature of untreated HIV infection suggesting a
significant contribution of Treg to the pathogenesis of
HIV disease. Their role may be two-edged: attenuating
HIV-induced immune hyperactivation while suppressing the
immune response to HIV and mucosal pathogens.
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