Bacterial toxins fuel disease progression in cutaneous T-cell lymphoma
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Bacterial toxins fuel disease progression in cutaneous T-cell lymphoma. / Willerslev-Olsen, Andreas; Krejsgaard, Thorbjørn; Lindahl, Lise Maria; Bonefeld, Charlotte Menne; Wasik, Mariusz A; Koralov, Sergei B; Geisler, Carsten; Kilian, Mogens; Iversen, Lars; Woetmann, Anders; Odum, Niels.
In: Toxins, Vol. 5, No. 8, 08.2013, p. 1402-21.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Bacterial toxins fuel disease progression in cutaneous T-cell lymphoma
AU - Willerslev-Olsen, Andreas
AU - Krejsgaard, Thorbjørn
AU - Lindahl, Lise Maria
AU - Bonefeld, Charlotte Menne
AU - Wasik, Mariusz A
AU - Koralov, Sergei B
AU - Geisler, Carsten
AU - Kilian, Mogens
AU - Iversen, Lars
AU - Woetmann, Anders
AU - Odum, Niels
PY - 2013/8
Y1 - 2013/8
N2 - In patients with cutaneous T-cell lymphoma (CTCL) bacterial infections constitute a major clinical problem caused by compromised skin barrier and a progressive immunodeficiency. Indeed, the majority of patients with advanced disease die from infections with bacteria, e.g., Staphylococcus aureus. Bacterial toxins such as staphylococcal enterotoxins (SE) have long been suspected to be involved in the pathogenesis in CTCL. Here, we review links between bacterial infections and CTCL with focus on earlier studies addressing a direct role of SE on malignant T cells and recent data indicating novel indirect mechanisms involving SE- and cytokine-driven cross-talk between malignant- and non-malignant T cells.
AB - In patients with cutaneous T-cell lymphoma (CTCL) bacterial infections constitute a major clinical problem caused by compromised skin barrier and a progressive immunodeficiency. Indeed, the majority of patients with advanced disease die from infections with bacteria, e.g., Staphylococcus aureus. Bacterial toxins such as staphylococcal enterotoxins (SE) have long been suspected to be involved in the pathogenesis in CTCL. Here, we review links between bacterial infections and CTCL with focus on earlier studies addressing a direct role of SE on malignant T cells and recent data indicating novel indirect mechanisms involving SE- and cytokine-driven cross-talk between malignant- and non-malignant T cells.
KW - Bacterial Infections
KW - Bacterial Toxins
KW - Cytokines
KW - Disease Progression
KW - Drug Resistance, Bacterial
KW - Enterotoxins
KW - Genes, T-Cell Receptor beta
KW - Humans
KW - Lymphoma, T-Cell, Cutaneous
KW - Morbidity
KW - Prevalence
KW - Skin Neoplasms
KW - Staphylococcus aureus
KW - T-Lymphocytes
U2 - 10.3390/toxins5081402
DO - 10.3390/toxins5081402
M3 - Journal article
C2 - 23949004
VL - 5
SP - 1402
EP - 1421
JO - Toxins
JF - Toxins
SN - 2072-6651
IS - 8
ER -
ID: 106272614