Expression of Epstein-Barr virus in cutaneous T-cell lymphoma including mycosis fungoides

Shimakage, Misuzu; Sasagawa, Toshiyuki; Kawahara, Katsunobu; Yutsudo, Masuo; Kusuoka, Hideo; Kozuka, Takehito

doi:10.1002/1097-0215(200102)9999:9999<::aid-ijc1172>3.0.co;2-o

Cited by 39 publications

(34 citation statements)

References 31 publications

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“…However, others have not been able to confirm these findings (Boni et al, 1996;Wood et al, 1996). Epstein -Barr virus infection has also been previously implicated in several kinds of lymphomas, including peripheral T-cell lymphomas (Shimakage et al, 2001;Kanegane et al, 2002). Another study showed significantly higher CMV seropositivity rates in early-stage MF patients with normal immune systems and minimal skin involvement compared with control subjects (Herne et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Mycosis fungoides: is it a Borrelia burgdorferi-associated disease?

et al. 2006

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Mycosis fungoides (MF) is the most frequently found cutaneous T-cell lymphoma with an unknown aetiology. Several aetiopathogenetic mechanisms have been postulated, including persistent viral or bacterial infections. We looked for evidence of Borrelia burgdorferi (Bb), the aetiologic agent of Lyme disease (LD), in a case study of MF patients from Northeastern Italy, an area with endemic LD. Polymerase chain reaction for the flagellin gene of Bb was used to study formalin-fixed paraffin-embedded lesional skin biopsies from 83 patients with MF and 83 sex-and age-matched healthy controls with homolocalised cutaneous nevi. Borrelia burgdorferi-specific sequence was detected in 15 out of 83 skin samples of patients with MF (18.1%), but in none out of 83 matched healthy controls (Po0.0001). The Bb positivity rates detected in this study support a possible role for Bb in the aetiopathogenesis of MF in a population endemic for LD.

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Section: Discussionmentioning

confidence: 99%

Mycosis fungoides: is it a Borrelia burgdorferi-associated disease?

et al. 2006

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“…These methods are a modified version of those that we reported previously. 5,[12][13][14][15][16][17][18][19] Indirect Immunofluorescence Staining Formalin-fixed, paraffin-embedded tissue tumor specimens and control tissue were cut into serial 4-m-thick sections. After dewaxing and dehydration, the sections were autoclaved in 10 mmol citrate buffer (pH 6.0) for 10 minutes at 120°C to detect EBNA2 and BZLF1.…”

Section: Mrna In Situ Hybridizationmentioning

confidence: 99%

“…These methods were described previously. 5,[12][13][14][15][16][17][18][19] Polymerase Chain Reaction DNA was extracted from several sections of formalinfixed, paraffin-embedded tissues. The EBER1 primer sequences were: 5' primer, 5'-AAAACATGCGGACCACCAGC-3' (nucleotide positions 6776-6795) and 3' primer, 5'-AGGAC-CTACGCTGCCCTAGA-3' (nucleotide positions 6648-6629).…”

Section: Mrna In Situ Hybridizationmentioning

confidence: 99%

Expression of Epstein-Barr virus in Langerhans? cell histiocytosis*1

Shimakage

2004

Human Pathology

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“…2,3 The factors that drive a T-cell clone to proliferate and to escape from the immune control are not clearly understood. The pathogenic role of viruses [4][5][6] ; other epidermal cells, such as keratinocytes and dendritic cells 7,8 ; or aberrant secretion or response to certain cytokines, such as transforming growth factor ␤ (TGF␤), interferon ␥ (IFN␥), and interleukin 10 (IL-10), [9][10][11] have been evoked. CTCL may also be considered a result of defective negative regulation of cell growth, survival, or both.…”

Section: Introductionmentioning

confidence: 99%

Engagement of ILT2/CD85j in Sézary syndrome cells inhibits their CD3/TCR signaling

Nikolova

Musette

Bagot

et al. 2002

Blood

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Extensive phenotype analysis of cutaneous T-cell lymphoma (CTCL) malignant cell lines revealed surface expression of receptors usually not detected on normal circulating CD4 ؉ CD45RO ؉ lymphocytes. We previously found that CTCL malignant cells express the killer cell immunoglobulinlike receptor (KIR) KIR3DL2/CD158k, whereas they fail to express the other KIRs. In the present study, we report for the first time that the CD85j/immunoglobulin (Ig)-like transcript 2 (ILT2) receptor is found on Sé zary cell lines and on circulating Sé zary malignant CD4 ؉ cells, while it is hardly detectable on circulating CD4 ؉ lymphocytes from healthy individuals. We demonstrate that ILT2 is functional on CTCL cells, as its triggering leads to the recruitment of Src homology 2 domaincontaining tyrosine phosphatase (SHP-1) and to the specific inhibition of CTCL malignant cell proliferation induced by CD3/T-cell receptor (TCR) stimulation. Interestingly, we found that separated CD4 ؉ ILT2 ؉ circulating malignant Sé zary cells are less susceptible to anti-CD3 monoclonal antibody (mAb)-induced cell death than autologous CD4 ؉ ILT2 ؊ lymphocytes. Therefore, the resistance to apoptosis of Sé zary cells may result from distinct mechanisms including cytokineinduced high levels of bcl-2 and specific expression of inhibitory receptors involved in lymphocyte survival. (Blood.

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Expression of Epstein-Barr virus in cutaneous T-cell lymphoma including mycosis fungoides

Cited by 39 publications

References 31 publications

Mycosis fungoides: is it a Borrelia burgdorferi-associated disease?

Mycosis fungoides: is it a Borrelia burgdorferi-associated disease?

Expression of Epstein-Barr virus in Langerhans? cell histiocytosis*1

Engagement of ILT2/CD85j in Sézary syndrome cells inhibits their CD3/TCR signaling

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