Sézary syndrome patients demonstrate a defect in dendritic cell populations: effects of CD40 ligand and treatment with GM-CSF on dendritic cell numbers and the production of cytokines

Wysocka, Maria; Zaki, Mohamed H.; French, Lars E.; Chehimi, Jihed; Shapiro, Michael B.; Everetts, Suzanne E.; McGinnis, Karen S.; Montaner, Luis J.; Rook, Alain H.

doi:10.1182/blood-2002-01-0231

Cited by 71 publications

(67 citation statements)

References 60 publications

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“…A reduction in circulating DC has also been reported in multiple myeloma, acute myeloid leukemia and Sezary syndrome. [15][16][17] These data and our findings indicate that a loss of BDC is a feature shared by different hematologic malignancies and suggest that common mechanisms to defective DC populations exist. VEGF, an important regulator of angiogenesis and hematopoiesis, is secreted in large amounts by a wide variety of hematopoietic tumors.…”

Section: Discussionsupporting

confidence: 58%

Defective blood dendritic cells in chronic myeloid leukemia correlate with high plasmatic VEGF and are not normalized by imatinib mesylate

Boissel

Rousselot²,

Raffoux³

et al. 2004

Leukemia

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Section: Discussionsupporting

confidence: 58%

Defective blood dendritic cells in chronic myeloid leukemia correlate with high plasmatic VEGF and are not normalized by imatinib mesylate

Boissel

Rousselot²,

Raffoux³

et al. 2004

Leukemia

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“…Other studies of immunosuppressed patients with APC defects identified a reduction in M CD11c ϩ DC precursors numbers concurrent with increases in more Mac-like M but normal in vitro 4ϩGM-induced differentiation of M to iDC (26,27). As seen in Fig.…”

Section: Patient M Differentiation To Idcmentioning

confidence: 56%

Failure of Monocytes of Trauma Patients to Convert to Immature Dendritic Cells is Related to Preferential Macrophage-Colony-Stimulating Factor-Driven Macrophage Differentiation

De¹,

Laudański²,

Miller-Graziano

2003

The Journal of Immunology

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Following trauma, increased inflammatory monokine activation and depressed APC function can occur simultaneously. These contradictory monocyte (Mφ) dysfunctions could result if postinjury Mφ differentiation preferentially favored inflammatory macrophage (Mac) differentiation over development into the most potent APC, dendritic cells (DC). In this report, Mφ of trauma patients with a depressed MLR induction capacity are, for the first time, shown to be unable to differentiate in vitro to immature CD1a+ DC under the influence of GM-CSF and IL-4. Trauma patient Mφ that retained MLR-inducing capacity had a nonsignificant reduction in DC differentiation capacity. Only patient Mφ populations with depressed differentiation to immature DC (iDC) demonstrated depressed IL-12 and IL-15 production and a continued reduced MLR induction capacity. Neither increased IL-10 production nor decreased CD11c+ DC precursor numbers correlated with depressed Mφ-to-DC differentiation. Instead, these patients’ APC-dysfunctional Mφ populations had increased expression of inflammatory Mac phenotypes (CD64+, CD86low, HLA-DRlow) and up-regulated secretion of M-CSF. M-CSF combined with IL-6 inhibits Mφ-to-iDC differentiation and promotes Mφ-to-Mac differentiation by down-regulating GM-CSFR expression and increasing DC apoptosis. Both depressed GM-CSFR expression and increased Mφ iDC apoptosis, as well as increased expression of CD126 (IL-6R) and CD115 (M-CSFR), were detected in APC-defective patient Mφ. In vitro addition of anti-M-CSF enhanced the IL-4 plus GM-CSF-induced Mφ-to-DC differentiation of these patients. This suggests that, in trauma patients, enhanced Mφ-to-Mac differentiation with concomitant inhibited iDC development is partially due to increased circulating Mφ sensitivity to and production of M-CSF and contributes to postinjury immunoaberrations.

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“…Approximately 50% of patients with CTCL, particularly those with advanced stage disease, will ultimately succumb to infectious complications [49][50][51]. Both quantitative and qualitative defects in natural killer (NK) cell [52,53], dendritic cell [54], and T cell-mediated [55][56][57] immunity are observed in CTCL. In addition, CTCL is associated with a significant loss of the T-cell repertoire, analogous to that observed in HIV infection.…”

Section: Immunopathogenesismentioning

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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Sézary syndrome patients demonstrate a defect in dendritic cell populations: effects of CD40 ligand and treatment with GM-CSF on dendritic cell numbers and the production of cytokines

Cited by 71 publications

References 60 publications

Defective blood dendritic cells in chronic myeloid leukemia correlate with high plasmatic VEGF and are not normalized by imatinib mesylate

Defective blood dendritic cells in chronic myeloid leukemia correlate with high plasmatic VEGF and are not normalized by imatinib mesylate

Failure of Monocytes of Trauma Patients to Convert to Immature Dendritic Cells is Related to Preferential Macrophage-Colony-Stimulating Factor-Driven Macrophage Differentiation

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

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