The Experts below are selected from a list of 384651 Experts worldwide ranked by ideXlab platform
A. Offidani - One of the best experts on this subject based on the ideXlab platform.
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Characterization and profiling of immunomodulatory genes in resident mesenchymal stem cells reflect the Th1-Th17/Th2 imbalance of psoriasis
Archives of Dermatological Research, 2014Co-Authors: A. Campanati, M. Orciani, V. Consales, R. Lazzarini, G. Ganzetti, G. Benedetto, R. Primio, A. OffidaniAbstract:The expression of genes encoding for Th1, Th2 and Th17 cytokines has been extensively evaluated in differentiated skin cells of psoriatic patients. The microenvironment exerts a control on the phenotype of resident mesenchymal stem cells (MSCs) into the skin of psoriasis patients. Aim of the study was to extensively evaluate the relative expression of 43 genes encoding for Th1, Th2 and Th17 cytokines in MSCs isolated from skin of psoriasis patients. MSCs resident into psoriatic skin were isolated, characterized and profiled by PCR array for the relative expression of genes encoding for cytokines involved in Th1, Th2 and Th17 pathways. MSCs isolated from the skin of healthy subjects were used as control. The MSCs isolated from skin of psoriasis patients showed a greater relative expression of the most part of the analyzed genes encoding for Th1 and Th17 cytokines: INF-γ, CCR5, CXCL9, CXCL10, IL6, IL8, TNF-α, IL23A, CCL2, CCL20, CXCL2, CXCL5, IL17C, IL17F, IL17RA, IL21, TLR2 than healthy subjects. On the contrary, the relative expression of genes encoding for Th2 cytokines: CCL1, CCL22, CXCL12, IL2, IL3, IL4, IL13B, IL 22, IL 27, TGF-β1, was similar between the MSCs isolated from psoriasis and healthy subjects. In conclusion, the MSCs isolated from psoriasis show an imbalance between the Th1-Th17 and Th2 pathways, which reflects the well-known abnormal balance observed in differentiated skin cells. This evidence could strengthen the hypothesis of an early involvement of resident MSCs in the pathogenesis of psoriasis.
Sizhou Feng - One of the best experts on this subject based on the ideXlab platform.
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Differential expression profile of Th1/Th17/Th2-related chemokines and their receptors in patients with acquired bone marrow failure syndromes.
Human immunology, 2012Co-Authors: Yizhou Zheng, Fang Chen, Dandan Chen, Yingqi Shao, Jun Shi, Sizhou FengAbstract:Th1/Th17/Th2-related chemokines (CXCL10/CCL20/CCL2) and their receptors (CXCR3/CCR6/CCR2) have rarely been studied in acquired bone marrow failure syndromes (BMFs). We evaluated the concentrations of CXCL10, CCL20 and CCL2 in plasma and BM fluid from aplastic anemia (AA), paroxysmal nocturnal hemoglobinuria (PNH), and myelodysplastic syndromes (MDS) patients by enzyme-linked immunosorbent assay (ELISA). Real-time quantitative polymerase chain reaction (RT-PCR) was performed to determine mRNA expressions of those chemokines and their receptors. CCL20 levels in both plasma and BM fluid from AA, PNH and MDS patients were significantly higher than those in the corresponding samples from healthy controls; there were no differences in terms of CXCL10 and CCL2 levels. Significantly higher expressions of CXCR3 and CCL20 mRNA, meanwhile significantly lower expression of CCR2 mRNA in both peripheral blood mononuclear cells (PBMNCs) and bone marrow MNCs (BMMNCs) from AA and PNH patients were observed, with no differences in terms of CXCL10, CCL2 and CCR6 mRNA expressions. CCR6 mRNA expressions in both PBMNCs and BMMNCs from MDS patients were significantly higher than of the corresponding samples from controls. Our study implicated that CXCL10-CXCR3, CCL20-CCR6 and CCL2-CCR2 interaction might play important roles in Th1 and Th17 (but not for Th2) cells trafficking toward BM in acquired bone marrow failure syndromes.
Shinji Kagami - One of the best experts on this subject based on the ideXlab platform.
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association of nerve growth factor chemokine c c motif ligands and immunoglobulin e with pruritus in cutaneous t cell lymphoma
Acta Dermato-venereologica, 2013Co-Authors: Hiraku Suga, Hideki Fujita, Shinji Kagami, Makoto Sugaya, Tomomitsu Miyagaki, Hanako Ohmatsu, Yoshihide Asano, Yayoi Tada, Takafumi Kadono, Shinichi SatoAbstract:Many patients with cutaneous T-cell lymphoma (CTCL) experience severe pruritus. This study evaluated serum levels of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in patients with CTCL. Although serum NGF and BDNF levels in patients with CTCL were not significantly higher than in healthy controls, serum NGF levels in patients with Sezary syndrome were higher than in those with mycosis fungoides and in healthy controls. Enhanced NGF expression by keratinocytes and increased dermal nerve fibres were detected in lesional skin of subjects with Sezary syndrome. Correlations between pruritus in CTCL and serum levels of NGF, BDNF, chemokine (C-C motif) ligand 1 (CCL1), CCL17, CCL26, CCL27, lactate dehydrogenase (LDH), IgE, and soluble interleukin-2 receptor were analysed. Serum CCL1, CCL26, LDH, and IgE levels correlated with pruritus in patients with CTCL. NGF may be associated with increased dermal nerve fibres and pruritus in Sezary syndrome, and CCL1, CCL26, and IgE may be associated with pruritus in CTCL.
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CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27
Experimental dermatology, 2006Co-Authors: Shinji Kagami, Mayumi Komine, Yuichiro Tsunemi, Hidehisa Saeki, Takashi Kakinuma, Koichiro Nakamura, K. Sasaki, Akihiko Asahina, Kunihiko TamakiAbstract:Both CCL27 and CCL28 are ligands for CCR10 and attract CCR10(+) lymphocytes. We previously demonstrated that CCL27 and CCL28 were strongly expressed in sera and lesional keratinocytes of patients with atopic dermatitis and psoriasis vulgaris. However, the regulation of CCL27 and CCL28 production in keratinocytes has not been well documented. In this study, we showed that CCL27 and CCL28 expression and production by a human keratinocyte cell line, HaCaT cells, were strongly induced by inflammatory cytokines tumor necrosis factor-alpha and interleukin-1beta. CCL27 production was downregulated by inhibitors of p38 mitogen-activated protein kinase and nuclear factor-kappa B (NF-kappaB). By contrast, CCL28 production was downregulated by inhibitors of extracellular signal-regulated kinase and NF-kappaB. Our study results suggest that CCL28 produced by keratinocytes is mediated by different signal pathways from CCL27 and that both CCL27 and CCL28 are involved in the pathogenesis of inflammatory skin diseases.
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significant elevation of serum levels of eotaxin 3 CCL26 but not of eotaxin 2 CCL24 in patients with atopic dermatitis serum eotaxin 3 CCL26 levels reflect the disease activity of atopic dermatitis
Clinical and Experimental Immunology, 2003Co-Authors: Shinji Kagami, Yuichiro Tsunemi, Tomonori Takekoshi, Megumi Kishimoto, Hidehisa Saeki, Hiroshi Mitsui, Takashi Kakinuma, Hideki Fujita, Koichiro Nakamura, Hideshi ToriiAbstract:Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease characterized by the predominant infiltration of T cells, eosinophils and macrophages in lesional skin. Recently, eotaxin-2/CCL24 and eotaxin-3/CCL26 were identified as CC chemokines that signal exclusively via the CCR3 receptor and have eosinophil-selective chemoattractant activity, as does eotaxin/CCL11. We previously reported that serum levels of thymus and activation-regulated chemokine (TARC)/CCL17 and macrophage-derived chemokine (MDC)/CCL22 were correlated with the severity of AD. In this report, we investigated the participation of eotaxin-2/CCL24 and eotaxin-3/CCL26 in AD, first measuring the serum levels of eotaxin-2/CCL24 and eotaxin-3/CCL26 in 30 patients with AD, 20 patients with psoriasis vulgaris and 20 healthy controls. The serum levels of eotaxin-3/CCL26 (but not eotaxin-2/CCL24) were significantly higher in patients with AD than in either healthy controls or patients with psoriasis vulgaris; furthermore, the eotaxin-3/CCL26 levels in patients with moderate and severe AD were significantly higher than eotaxin-3/CCL26 levels in patients with mild AD. The serum eotaxin-3/CCL26 levels tended to decrease after treatment, but there was no significant difference between groups. Moreover, the serum eotaxin-3/CCL26 levels were significantly correlated with the serum TARC/CCL17 and MDC/CCL22 levels, eosinophil numbers in peripheral blood and the scoring AD (SCORAD) index. Our study strongly suggests that serum levels of eotaxin-3/CCL26, but not of eotaxin-2/CCL24, have a notable correlation with disease activity of AD and that eotaxin-3/CCL26, as well as TARC/CCL17 and MDC/CCL22, may be involved in the pathogenesis of AD.
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Significant elevation of serum levels of eotaxin‐3/CCL26, but not of eotaxin‐2/CCL24, in patients with atopic dermatitis: serum eotaxin‐3/CCL26 levels reflect the disease activity of atopic dermatitis
Clinical and Experimental Immunology, 2003Co-Authors: Shinji Kagami, Yuichiro Tsunemi, Tomonori Takekoshi, Megumi Kishimoto, Hidehisa Saeki, Hiroshi Mitsui, Takashi Kakinuma, Hideki Fujita, Koichiro Nakamura, Hideshi ToriiAbstract:Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease characterized by the predominant infiltration of T cells, eosinophils and macrophages in lesional skin. Recently, eotaxin-2/CCL24 and eotaxin-3/CCL26 were identified as CC chemokines that signal exclusively via the CCR3 receptor and have eosinophil-selective chemoattractant activity, as does eotaxin/CCL11. We previously reported that serum levels of thymus and activation-regulated chemokine (TARC)/CCL17 and macrophage-derived chemokine (MDC)/CCL22 were correlated with the severity of AD. In this report, we investigated the participation of eotaxin-2/CCL24 and eotaxin-3/CCL26 in AD, first measuring the serum levels of eotaxin-2/CCL24 and eotaxin-3/CCL26 in 30 patients with AD, 20 patients with psoriasis vulgaris and 20 healthy controls. The serum levels of eotaxin-3/CCL26 (but not eotaxin-2/CCL24) were significantly higher in patients with AD than in either healthy controls or patients with psoriasis vulgaris; furthermore, the eotaxin-3/CCL26 levels in patients with moderate and severe AD were significantly higher than eotaxin-3/CCL26 levels in patients with mild AD. The serum eotaxin-3/CCL26 levels tended to decrease after treatment, but there was no significant difference between groups. Moreover, the serum eotaxin-3/CCL26 levels were significantly correlated with the serum TARC/CCL17 and MDC/CCL22 levels, eosinophil numbers in peripheral blood and the scoring AD (SCORAD) index. Our study strongly suggests that serum levels of eotaxin-3/CCL26, but not of eotaxin-2/CCL24, have a notable correlation with disease activity of AD and that eotaxin-3/CCL26, as well as TARC/CCL17 and MDC/CCL22, may be involved in the pathogenesis of AD.
A. Campanati - One of the best experts on this subject based on the ideXlab platform.
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Characterization and profiling of immunomodulatory genes in resident mesenchymal stem cells reflect the Th1-Th17/Th2 imbalance of psoriasis
Archives of Dermatological Research, 2014Co-Authors: A. Campanati, M. Orciani, V. Consales, R. Lazzarini, G. Ganzetti, G. Benedetto, R. Primio, A. OffidaniAbstract:The expression of genes encoding for Th1, Th2 and Th17 cytokines has been extensively evaluated in differentiated skin cells of psoriatic patients. The microenvironment exerts a control on the phenotype of resident mesenchymal stem cells (MSCs) into the skin of psoriasis patients. Aim of the study was to extensively evaluate the relative expression of 43 genes encoding for Th1, Th2 and Th17 cytokines in MSCs isolated from skin of psoriasis patients. MSCs resident into psoriatic skin were isolated, characterized and profiled by PCR array for the relative expression of genes encoding for cytokines involved in Th1, Th2 and Th17 pathways. MSCs isolated from the skin of healthy subjects were used as control. The MSCs isolated from skin of psoriasis patients showed a greater relative expression of the most part of the analyzed genes encoding for Th1 and Th17 cytokines: INF-γ, CCR5, CXCL9, CXCL10, IL6, IL8, TNF-α, IL23A, CCL2, CCL20, CXCL2, CXCL5, IL17C, IL17F, IL17RA, IL21, TLR2 than healthy subjects. On the contrary, the relative expression of genes encoding for Th2 cytokines: CCL1, CCL22, CXCL12, IL2, IL3, IL4, IL13B, IL 22, IL 27, TGF-β1, was similar between the MSCs isolated from psoriasis and healthy subjects. In conclusion, the MSCs isolated from psoriasis show an imbalance between the Th1-Th17 and Th2 pathways, which reflects the well-known abnormal balance observed in differentiated skin cells. This evidence could strengthen the hypothesis of an early involvement of resident MSCs in the pathogenesis of psoriasis.
Yizhou Zheng - One of the best experts on this subject based on the ideXlab platform.
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Differential expression profile of Th1/Th17/Th2-related chemokines and their receptors in patients with acquired bone marrow failure syndromes.
Human immunology, 2012Co-Authors: Yizhou Zheng, Fang Chen, Dandan Chen, Yingqi Shao, Jun Shi, Sizhou FengAbstract:Th1/Th17/Th2-related chemokines (CXCL10/CCL20/CCL2) and their receptors (CXCR3/CCR6/CCR2) have rarely been studied in acquired bone marrow failure syndromes (BMFs). We evaluated the concentrations of CXCL10, CCL20 and CCL2 in plasma and BM fluid from aplastic anemia (AA), paroxysmal nocturnal hemoglobinuria (PNH), and myelodysplastic syndromes (MDS) patients by enzyme-linked immunosorbent assay (ELISA). Real-time quantitative polymerase chain reaction (RT-PCR) was performed to determine mRNA expressions of those chemokines and their receptors. CCL20 levels in both plasma and BM fluid from AA, PNH and MDS patients were significantly higher than those in the corresponding samples from healthy controls; there were no differences in terms of CXCL10 and CCL2 levels. Significantly higher expressions of CXCR3 and CCL20 mRNA, meanwhile significantly lower expression of CCR2 mRNA in both peripheral blood mononuclear cells (PBMNCs) and bone marrow MNCs (BMMNCs) from AA and PNH patients were observed, with no differences in terms of CXCL10, CCL2 and CCR6 mRNA expressions. CCR6 mRNA expressions in both PBMNCs and BMMNCs from MDS patients were significantly higher than of the corresponding samples from controls. Our study implicated that CXCL10-CXCR3, CCL20-CCR6 and CCL2-CCR2 interaction might play important roles in Th1 and Th17 (but not for Th2) cells trafficking toward BM in acquired bone marrow failure syndromes.