T lymphocytes from Sézary syndrome patients express β1 integrins whose β(1–6)-branched N-linked oligosaccharides reflect their adhesive capacity

Braut-Boucher, F.; Font, J.; Pichon, J.; Paulin, Yolene; Boukhelifa, Malika; Auger, Michèle; Derappe, Christian

doi:10.1016/s0145-2126(98)00094-0

Cited by 9 publications

(2 citation statements)

References 24 publications

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“…1D). This was consistent with prior reports of Sezary cells bearing the branched N-glycans recognized by PHA (47,48). Strong PHA reactivity was also seen on other cells within the dermis and epidermis.…”

Section: Glycosylation Patterns In Mycosis Fungoides Lesionssupporting

confidence: 94%

Galectin-1–Mediated Apoptosis in Mycosis Fungoides: The Roles of CD7 and Cell Surface Glycosylation

et al. 2003

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Sezary cells, the malignant T cells in mycosis fungoides/Sezary syndrome, resist a variety of apoptosis-inducing agents, a feature that contributes to the poor response to therapy in mycosis fungoides. Galectin-1 is a mammalian lectin that triggers T cell apoptosis. For T cells to be susceptible to galectin-1-induced apoptosis, the T cells must express specific glycoprotein receptors, such as CD7, that bear the specific oligosaccharides recognized by galectin-1. Because Sezary cells are characteristically CD7 ؊ , lack of CD7 expression has been proposed to render Sezary cells resistant to galectin-1-induced death. However, the role played by aberrant cell surface glycosylation in resistance of Sezary cells to galectin-1 has not been examined. In this study, we demonstrated abundant galectin-1 in mycosis fungoides skin lesions, indicating that Sezary cells are exposed to galectin-1 in vivo. To determine specific characteristics of Sezary cells that contribute to galectin-1 resistance, we assessed CD7 expression and cell surface glycosylation of Sezary cells in mycosis fungoides lesions and of four Sezary T cell lines. Sezary cells in primary lesions and Sezary T cell lines demonstrated a characteristic "glycotype" with sialylated core 1 O-glycans that promote galectin-1 resistance. Expression of CD7 was necessary but not sufficient for galectin-1-induced death of Sezary cell lines. In addition, CD7 ؊ Sezary cell lines, and Sezary cells within mycosis fungoides lesions, expressed galectin-1, whereas CD7-positive Sezary cell lines did not express galectin-1. We propose that both loss of CD7 expression and altered cellular glycosylation contribute to apoptosis resistance of malignant T cells in mycosis fungoides.

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