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Depletion and impaired interferon‐ α ‐producing capacity of blood plasmacytoid dendritic cells in human T‐cell leukaemia virus type I‐infected individuals
Author(s) -
Hishizawa Masakatsu,
Imada Kazunori,
Kitawaki Toshio,
Ueda Maki,
Kadowaki Norimitsu,
Uchiyama Takashi
Publication year - 2004
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2004.04956.x
Subject(s) - immunology , plasmacytoid dendritic cell , peripheral blood mononuclear cell , interferon , biology , dendritic cell , asymptomatic carrier , virology , acquired immune system , immunity , virus , asymptomatic , immune system , medicine , in vitro , biochemistry
Summary Dendritic cells (DCs) play an important role in innate and adaptive immunity. There are two major populations of blood DCs, myeloid DCs (myDCs) and plasmacytoid DCs (pcDCs). pcDCs are particularly important in antiviral as well as in general host defence, as they are the principal producers of type I interferons (IFNs). In this study, we analysed myDCs and pcDCs in healthy controls, human T‐cell leukaemia virus type I (HTLV‐I)‐infected asymptomatic carriers (ACs), and patients with adult T‐cell leukaemia (ATL). ATL patients had significantly decreased number of pcDCs and myDCs compared with controls. IFN‐ α production by peripheral blood mononuclear cells (PBMCs) was markedly reduced in ATL patients. Purified pcDCs from ACs were found to have impaired IFN‐ α ‐producing capacity, suggesting a functional defect in pcDCs in HTLV‐I‐infected individuals. Interestingly, pcDCs were shown to be susceptible to HTLV‐I infection. Thus, impaired IFN‐ α production by pcDCs may contribute to the immunodeficiency observed in ATL. Furthermore, IFN‐ α ‐producing capacity was inversely correlated with HTLV‐I proviral load in PBMCs from ACs, suggesting a role for pcDCs in maintaining the carrier state. Taken together, we hypothesize that the depletion and impaired IFN‐ α ‐producing capacity of blood DCs may contribute to the immunodeficiency in ATL and/or the development of ATL.