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Blood, 15 February 2005, Vol. 105, No. 4, pp. 1640-1647.
Prepublished online as a Blood First Edition Paper on October 28, 2004; DOI 10.1182/blood-2004-06-2181.
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IMMUNOBIOLOGY
Cutaneous T-cell lymphoma: malignant proliferation of T-regulatory cells
Carole L. Berger,
Robert Tigelaar,
Justine Cohen,
Kavita Mariwalla,
Jennifer Trinh,
Nianci Wang, and
Richard L. Edelson
From the Department of Dermatology, Yale University School of Medicine, New Haven, CT.
Studies in an in vitro model of cutaneous T-cell lymphoma (CTCL) demonstrated that CTCL cell proliferation is stimulated by direct contact with autologous, immature dendritic cells (DCs), suggesting that CD4+ CTCL cell division is driven by antigens presented by DC major histocompatibility complex (MHC) class 2. We now report that the T-cell receptor (TCR) of the CD4+ CTCL cells is triggered after interaction with DCs loaded with apoptotic CTCL cells, as shown by reduced membrane expression of CD3 and the TCR, up-regulation of cytotoxic T lymphocyte antigen-4 (CTLA-4), and calcium mobilization. CTCL cells adopt a T-regulatory (Treg) phenotype expressing CD25/CTLA-4 and FoxP3 and secreting interleukin-10 (IL-10) and transforming growth factor- (TGF-). Treg CTCL cells suppress normal T-cell antigen-driven secretion of IL-2 and interferon- (IFN-). Blocking DC MHC class 2 expression or transport inhibited CTCL cell adoption of a Treg phenotype. Allogeneic CTCL cells or normal CD4 T cells served as sources of apoptotic material for CTCL cell conversion to a Treg phenotype. Conversion of CTCL cells to Treg cells may explain the anergic, immunosuppressive nature of the malignancy. (Blood. 2005;105:1640-1647)
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