The Experts below are selected from a list of 2640 Experts worldwide ranked by ideXlab platform

Agnes Doreau - One of the best experts on this subject based on the ideXlab platform.

  • interleukin 17 acts in synergy with b cell activating Factor to influence b cell biology and the pathophysiology of systemic lupus erythematosus
    Nature Immunology, 2009
    Co-Authors: Agnes Doreau, Alexandre Belot, Jeremy Bastid, Benjamin Riche, Marieclaude Trescolbiemont, Bruno Ranchin
    Abstract:

    How interleukin 17 influences B cell biology is unclear. Bonnefoy-Berard and colleagues find that interleukin 17 alone or in combination with B cell–activating Factor controls the survival, proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. Studies have suggested involvement of interleukin 17 (IL-17) in autoimmune diseases, although its effect on B cell biology has not been clearly established. Here we demonstrate that IL-17 alone or in combination with B cell–activating Factor controlled the survival and proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. This effect was mediated mainly through the nuclear Factor-κB-regulated Transcription Factor Twist-1. In support of the relevance of our observations and the potential involvement of IL-17 in B cell biology, we found that the serum of patients with systemic lupus erythematosus had higher concentrations of IL-17 than did the serum of healthy people and that IL-17 abundance correlated with the disease severity of systemic lupus erythematosus.

  • interleukin 17 acts in synergy with b cell activating Factor to influence b cell biology and the pathophysiology of systemic lupus erythematosus
    Nature Immunology, 2009
    Co-Authors: Agnes Doreau, Alexandre Belot, Jeremy Bastid, Benjamin Riche, Marieclaude Trescolbiemont, Bruno Ranchin, Nicole Fabien
    Abstract:

    Studies have suggested involvement of interleukin 17 (IL-17) in autoimmune diseases, although its effect on B cell biology has not been clearly established. Here we demonstrate that IL-17 alone or in combination with B cell-activating Factor controlled the survival and proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. This effect was mediated mainly through the nuclear Factor-kappaB-regulated Transcription Factor Twist-1. In support of the relevance of our observations and the potential involvement of IL-17 in B cell biology, we found that the serum of patients with systemic lupus erythematosus had higher concentrations of IL-17 than did the serum of healthy people and that IL-17 abundance correlated with the disease severity of systemic lupus erythematosus.

Marieclaude Trescolbiemont - One of the best experts on this subject based on the ideXlab platform.

  • interleukin 17 acts in synergy with b cell activating Factor to influence b cell biology and the pathophysiology of systemic lupus erythematosus
    Nature Immunology, 2009
    Co-Authors: Agnes Doreau, Alexandre Belot, Jeremy Bastid, Benjamin Riche, Marieclaude Trescolbiemont, Bruno Ranchin
    Abstract:

    How interleukin 17 influences B cell biology is unclear. Bonnefoy-Berard and colleagues find that interleukin 17 alone or in combination with B cell–activating Factor controls the survival, proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. Studies have suggested involvement of interleukin 17 (IL-17) in autoimmune diseases, although its effect on B cell biology has not been clearly established. Here we demonstrate that IL-17 alone or in combination with B cell–activating Factor controlled the survival and proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. This effect was mediated mainly through the nuclear Factor-κB-regulated Transcription Factor Twist-1. In support of the relevance of our observations and the potential involvement of IL-17 in B cell biology, we found that the serum of patients with systemic lupus erythematosus had higher concentrations of IL-17 than did the serum of healthy people and that IL-17 abundance correlated with the disease severity of systemic lupus erythematosus.

  • interleukin 17 acts in synergy with b cell activating Factor to influence b cell biology and the pathophysiology of systemic lupus erythematosus
    Nature Immunology, 2009
    Co-Authors: Agnes Doreau, Alexandre Belot, Jeremy Bastid, Benjamin Riche, Marieclaude Trescolbiemont, Bruno Ranchin, Nicole Fabien
    Abstract:

    Studies have suggested involvement of interleukin 17 (IL-17) in autoimmune diseases, although its effect on B cell biology has not been clearly established. Here we demonstrate that IL-17 alone or in combination with B cell-activating Factor controlled the survival and proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. This effect was mediated mainly through the nuclear Factor-kappaB-regulated Transcription Factor Twist-1. In support of the relevance of our observations and the potential involvement of IL-17 in B cell biology, we found that the serum of patients with systemic lupus erythematosus had higher concentrations of IL-17 than did the serum of healthy people and that IL-17 abundance correlated with the disease severity of systemic lupus erythematosus.

Jeremy Bastid - One of the best experts on this subject based on the ideXlab platform.

  • interleukin 17 acts in synergy with b cell activating Factor to influence b cell biology and the pathophysiology of systemic lupus erythematosus
    Nature Immunology, 2009
    Co-Authors: Agnes Doreau, Alexandre Belot, Jeremy Bastid, Benjamin Riche, Marieclaude Trescolbiemont, Bruno Ranchin
    Abstract:

    How interleukin 17 influences B cell biology is unclear. Bonnefoy-Berard and colleagues find that interleukin 17 alone or in combination with B cell–activating Factor controls the survival, proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. Studies have suggested involvement of interleukin 17 (IL-17) in autoimmune diseases, although its effect on B cell biology has not been clearly established. Here we demonstrate that IL-17 alone or in combination with B cell–activating Factor controlled the survival and proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. This effect was mediated mainly through the nuclear Factor-κB-regulated Transcription Factor Twist-1. In support of the relevance of our observations and the potential involvement of IL-17 in B cell biology, we found that the serum of patients with systemic lupus erythematosus had higher concentrations of IL-17 than did the serum of healthy people and that IL-17 abundance correlated with the disease severity of systemic lupus erythematosus.

  • interleukin 17 acts in synergy with b cell activating Factor to influence b cell biology and the pathophysiology of systemic lupus erythematosus
    Nature Immunology, 2009
    Co-Authors: Agnes Doreau, Alexandre Belot, Jeremy Bastid, Benjamin Riche, Marieclaude Trescolbiemont, Bruno Ranchin, Nicole Fabien
    Abstract:

    Studies have suggested involvement of interleukin 17 (IL-17) in autoimmune diseases, although its effect on B cell biology has not been clearly established. Here we demonstrate that IL-17 alone or in combination with B cell-activating Factor controlled the survival and proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. This effect was mediated mainly through the nuclear Factor-kappaB-regulated Transcription Factor Twist-1. In support of the relevance of our observations and the potential involvement of IL-17 in B cell biology, we found that the serum of patients with systemic lupus erythematosus had higher concentrations of IL-17 than did the serum of healthy people and that IL-17 abundance correlated with the disease severity of systemic lupus erythematosus.

Alexandre Belot - One of the best experts on this subject based on the ideXlab platform.

  • interleukin 17 acts in synergy with b cell activating Factor to influence b cell biology and the pathophysiology of systemic lupus erythematosus
    Nature Immunology, 2009
    Co-Authors: Agnes Doreau, Alexandre Belot, Jeremy Bastid, Benjamin Riche, Marieclaude Trescolbiemont, Bruno Ranchin
    Abstract:

    How interleukin 17 influences B cell biology is unclear. Bonnefoy-Berard and colleagues find that interleukin 17 alone or in combination with B cell–activating Factor controls the survival, proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. Studies have suggested involvement of interleukin 17 (IL-17) in autoimmune diseases, although its effect on B cell biology has not been clearly established. Here we demonstrate that IL-17 alone or in combination with B cell–activating Factor controlled the survival and proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. This effect was mediated mainly through the nuclear Factor-κB-regulated Transcription Factor Twist-1. In support of the relevance of our observations and the potential involvement of IL-17 in B cell biology, we found that the serum of patients with systemic lupus erythematosus had higher concentrations of IL-17 than did the serum of healthy people and that IL-17 abundance correlated with the disease severity of systemic lupus erythematosus.

  • interleukin 17 acts in synergy with b cell activating Factor to influence b cell biology and the pathophysiology of systemic lupus erythematosus
    Nature Immunology, 2009
    Co-Authors: Agnes Doreau, Alexandre Belot, Jeremy Bastid, Benjamin Riche, Marieclaude Trescolbiemont, Bruno Ranchin, Nicole Fabien
    Abstract:

    Studies have suggested involvement of interleukin 17 (IL-17) in autoimmune diseases, although its effect on B cell biology has not been clearly established. Here we demonstrate that IL-17 alone or in combination with B cell-activating Factor controlled the survival and proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. This effect was mediated mainly through the nuclear Factor-kappaB-regulated Transcription Factor Twist-1. In support of the relevance of our observations and the potential involvement of IL-17 in B cell biology, we found that the serum of patients with systemic lupus erythematosus had higher concentrations of IL-17 than did the serum of healthy people and that IL-17 abundance correlated with the disease severity of systemic lupus erythematosus.

Robert A Weinberg - One of the best experts on this subject based on the ideXlab platform.

  • tumour invasion and metastasis initiated by microrna 10b in breast cancer
    Nature, 2007
    Co-Authors: Julie Teruyafeldstein, Robert A Weinberg
    Abstract:

    MicroRNAs have been implicated in regulating diverse cellular pathways. Although there is emerging evidence that some microRNAs can function as oncogenes or tumour suppressors, the role of microRNAs in mediating cancer metastasis remains unexplored. Here we show, using a combination of mouse and human cells, that microRNA-10b (miR-10b) is highly expressed in metastatic breast cancer cells and positively regulates cell migration and invasion. Overexpression of miR-10b in otherwise non-metastatic breast tumours initiates robust invasion and metastasis. Expression of miR-10b is induced by the Transcription Factor Twist, which binds directly to the putative promoter of mir-10b (MIRN10B). The miR-10b induced by Twist proceeds to inhibit translation of the messenger RNA encoding homeobox D10, resulting in increased expression of a well-characterized pro-metastatic gene, RHOC. Significantly, the level of miR-10b expression in primary breast carcinomas correlates with clinical progression. These findings suggest the workings of an undescribed regulatory pathway, in which a pleiotropic Transcription Factor induces expression of a specific microRNA, which suppresses its direct target and in turn activates another pro-metastatic gene, leading to tumour cell invasion and metastasis.

  • tumour invasion and metastasis initiated by microrna 10b in breast cancer
    Nature, 2007
    Co-Authors: Julie Teruyafeldstein, Robert A Weinberg
    Abstract:

    MicroRNAs have been implicated in regulating diverse cellular pathways. Although there is emerging evidence that some microRNAs can function as oncogenes or tumour suppressors, the role of microRNAs in mediating cancer metastasis remains unexplored. Here we show, using a combination of mouse and human cells, that microRNA-10b (miR-10b) is highly expressed in metastatic breast cancer cells and positively regulates cell migration and invasion. Overexpression of miR-10b in otherwise non-metastatic breast tumours initiates robust invasion and metastasis. Expression of miR-10b is induced by the Transcription Factor Twist, which binds directly to the putative promoter of mir-10b (MIRN10B). The miR-10b induced by Twist proceeds to inhibit translation of the messenger RNA encoding homeobox D10, resulting in increased expression of a well-characterized pro-metastatic gene, RHOC. Significantly, the level of miR-10b expression in primary breast carcinomas correlates with clinical progression. These findings suggest the workings of an undescribed regulatory pathway, in which a pleiotropic Transcription Factor induces expression of a specific microRNA, which suppresses its direct target and in turn activates another pro-metastatic gene, leading to tumour cell invasion and metastasis. A microRNA that may facilitate the movement of cells from one part of the embryo to another in its normal role has been found to be highly expressed in aggressive human breast cancers and to mediate breast cancer cell migration, invasion and metastasis. MicroRNAs, naturally occurring single-stranded RNA molecules involved in gene regulation, have been implicated previously in causing cancers, but this is the first report of a link to metastasis. The functional target of the microRNA appears to be the HOXD10 gene, one of the Hox gene family involved in directing embryo development. miR-10b is highly expressed in aggressive human breast cancers and mediates breast cancer cell migration, invasion and metastasis. miR-10b is Transcriptionally activated by Twist and exerts its effects by regulating the target genes HOXD10 and RHOC.