Th2 Cytokine mRNA Expression in Skin in Cutaneous T-Cell Lymphoma

Vowels, Benjamin R.; Lessin, Stuart R.; Cassin, Maureen; Jaworsky, Christine; Benoit, Bernice M.; Wolfe, Jonathan; Rook, Alain H.

doi:10.1111/1523-1747.ep12398454

Cited by 246 publications

(192 citation statements)

References 31 publications

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“…The expression of CCR4 in all cases of cutaneous ALCL and LyP is consistent with the hypothesis that CTCL are characterized by a Th2-like cytokine profile (19,20). With respect to cutaneous CD30ϩ lymphoproliferations, one study indeed showed increased expression of Th2 cytokines by transcription analysis (21).…”

Section: /11 T-nhl Not Otherwise Specified [Data Not Shown])supporting

confidence: 81%

Differential Expression of Thymus and Activation Regulated Chemokine and Its Receptor CCR4 in Nodal and Cutaneous Anaplastic Large-Cell Lymphomas and Hodgkin’s Disease

et al. 2002

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Section: /11 T-nhl Not Otherwise Specified [Data Not Shown])supporting

confidence: 81%

Differential Expression of Thymus and Activation Regulated Chemokine and Its Receptor CCR4 in Nodal and Cutaneous Anaplastic Large-Cell Lymphomas and Hodgkin’s Disease

et al. 2002

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“…Of note, MF/SS is associated with the expression of Th2-associated genes (e.g., GATA-3) and the production of Th2-associated cytokines (e.g., IL-4, IL-5, and IL-10), thus raising the possibility that a significant subset of patients may harbor Th2-derived clones [32][33][34][35][36]. As the cell of origin is further defined in subsets of CTCL, including MF/SS, one may anticipate that this data may have a significant impact on the classification, risk-stratification, and treatment of these diseases.…”

Section: Cell Of Originmentioning

confidence: 99%

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Wilcox

2011

American J Hematol

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Disease overview: Cutaneous T‐cell lymphomas are a heterogenous group of T‐cell lymphoproliferative disorders involving the skin, the majority of which may be classified as Mycosis fungoides (MF) or Sézary syndrome (SS).Diagnosis: The diagnosis of MF or SS requires the integration of clinical and histopathologic data.Risk‐adapted therapy: Tumor, node, metastasis, and blood (TNMB) staging remains the most important prognostic factor in MF/SS and forms the basis for a “risk‐adapted,” multidisciplinary approach to treatment. For patients with disease limited to the skin, expectant management or skin‐directed therapies is preferred, as both disease‐specific and overall survival for these patients is favorable. In contrast, patients with advanced‐stage disease with significant nodal, visceral, or blood involvement are generally approached with biologic‐response modifiers, denileukin diftitox, and histone deacetylase inhibitors before escalating therapy to include systemic, single‐agent chemotherapy. Multiagent chemotherapy may be used for those patients with extensive visceral involvement requiring rapid disease control. In highly‐selected patients with disease refractory to standard treatments, allogeneic stem‐cell transplantation may be considered. Am. J. Hematol., 2011. © 2011 Wiley‐Liss, Inc.

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“…6 In the early stages of the disease, the infiltrate consists primarily of non-malignant T helper 1 (T H 1) cells and cytotoxic CD8 þ T cells, which appear to control the malignant T cells through inhibitory cytokines, such as interferon (IFN)-a and IFN-g, and cytotoxicity directed against malignant T cells expressing tumorassociated antigens. [7][8][9] In later stages of the disease, the malignant T cells show aberrant hyperactivation of Janus kinase-3 (Jak3) 10 and signal tranducers and activators of transcription (STAT) 11,12 proteins, which in turn trigger survival signals and the expression of suppressor of cytokine signalling-3 (SOCS3). 13 SOCS3 protects the malignant T cells from inhibition by IFNs 13 and is a marker of a poor prognosis.…”

Section: Introductionmentioning

confidence: 99%

Malignant Tregs express low molecular splice forms of FOXP3 in Sézary syndrome

et al. 2008

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Sé zary syndrome (SS) is an aggressive variant of cutaneous T-cell lymphoma. During disease progression, immunodeficiency develops; however, the underlying molecular and cellular mechanisms are not fully understood. Here, we study the regulatory T cell (Treg) function and the expression of FOXP3 in SS. We demonstrate that malignant T cells in 8 of 15 patients stain positive with an anti-FOXP3 antibody. Western blotting analysis shows expression of two low molecular splice forms of FOXP3, but not of wild-type (wt) FOXP3. The malignant T cells produce interleukin-10 and TGF-b and suppress the growth of non-malignant T cells. The Treg phenotype and the production of suppressive cytokines are driven by aberrant activation of Jak3 independent of the FOXP3 splice forms. In contrast to wt FOXP3, the low molecular splice forms of FOXP3 have no inhibitory effect on nuclear factor-jB (NF-jB) activity in reporter assays which is in keeping with a constitutive NF-jB activity in the malignant T cells. In conclusion, we show that the malignant T cells express low molecular splice forms of FOXP3 and function as Tregs. Furthermore, we provide evidence that FOXP3 splice forms are functionally different from wt FOXP3 and not involved in the execution of the suppressive function. Thus, this is the first description of FOXP3 splice forms in human disease.

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Th2 Cytokine mRNA Expression in Skin in Cutaneous T-Cell Lymphoma

Cited by 246 publications

References 31 publications

Differential Expression of Thymus and Activation Regulated Chemokine and Its Receptor CCR4 in Nodal and Cutaneous Anaplastic Large-Cell Lymphomas and Hodgkin’s Disease

Differential Expression of Thymus and Activation Regulated Chemokine and Its Receptor CCR4 in Nodal and Cutaneous Anaplastic Large-Cell Lymphomas and Hodgkin’s Disease

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Malignant Tregs express low molecular splice forms of FOXP3 in Sézary syndrome

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