The Experts below are selected from a list of 47172 Experts worldwide ranked by ideXlab platform

Irun R. Cohen - One of the best experts on this subject based on the ideXlab platform.

  • heat shock protein 60 enhances cd4 cd25 regulatory t cell function via innate tlr2 signaling
    Journal of Clinical Investigation, 2006
    Co-Authors: Alexandra Zaninzhorov, Liora Cahalon, Raanan Margalit, Ofer Lider, Guy Tal, Irun R. Cohen
    Abstract:

    CD4+CD25+ Tregs regulate immunity, but little is known about their own regulation. We now report that the human 60-kDa heat shock protein (HSP60) acts as a costimulator of human Tregs, both CD4+CD25int and CD4+CD25hi. Treatment of Tregs with HSP60, or its peptide p277, before anti-CD3 activation significantly enhanced the ability of relatively low concentrations of the Tregs to downregulate CD4+CD25- or CD8+ target T cells, detected as inhibition of target T cell proliferation and IFN-gamma and TNF-alpha secretion. The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K, and p38, and were further enhanced by inhibition of ERK. HSP60-treated Tregs suppressed target T cells both by cell-to-cell contact and by secretion of TGF-beta and IL-10. In addition, the expression of ERK, NF-kappaB, and T-bet by downregulated target T cells was inhibited. Thus, HSP60, a Self-Molecule, can downregulate adaptive immune responses by upregulating Tregs innately through TLR2 signaling.

  • heat shock protein 60 enhances cd4 cd25 regulatory t cell function via innate tlr2 signaling
    Journal of Clinical Investigation, 2006
    Co-Authors: Alexandra Zaninzhorov, Liora Cahalon, Raanan Margalit, Ofer Lider, Irun R. Cohen
    Abstract:

    CD4+CD25+ Tregs regulate immunity, but little is known about their own regulation. We now report that the human 60-kDa heat shock protein (HSP60) acts as a costimulator of human Tregs, both CD4+CD25int and CD4+CD25hi. Treatment of Tregs with HSP60, or its peptide p277, before anti-CD3 activation significantly enhanced the ability of relatively low concentrations of the Tregs to downregulate CD4+CD25– or CD8+ target T cells, detected as inhibition of target T cell proliferation and IFN-γ and TNF-α secretion. The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K, and p38, and were further enhanced by inhibition of ERK. HSP60-treated Tregs suppressed target T cells both by cell-to-cell contact and by secretion of TGF-β and IL-10. In addition, the expression of ERK, NF-κB, and T-bet by downregulated target T cells was inhibited. Thus, HSP60, a Self-Molecule, can downregulate adaptive immune responses by upregulating Tregs innately through TLR2 signaling.

  • Autoimmunization to epidermal growth factor, a component of the immunological homunculus.
    Autoimmunity Reviews, 2002
    Co-Authors: Gisela Gonzalez, Enrique Montero, Kalet León, Irun R. Cohen, Agustin Lage
    Abstract:

    Abstract Epidermal growth factor (EGF) is being tried as a vaccine in cancer immunotherapy with the aim of inducing neutralizing antibodies that might affect EGF-dependent tumors. Here we summarize our experience using the EGF Self-Molecule as an autoimmunigen. We report here that IgG anti-EGF antibodies are prevalent in healthy people and that augmentation of the response to EGF requires conjugation to an effective carrier and an adjuvant. Paradoxically, the response to EGF immunization could be enhanced by an ‘immunosuppressive’ treatment with cyclophosphamide, most probably by suppressing active control mechanisms. EGF is expressed in the thymus. Thus, EGF may be added to the immunological homunculus, the class of Self-antigens to which there is both natural autoimmunity and natural regulation of the autoimmunity. The results using EGF as a vaccine can teach us about the homunculus and how to activate it.

Alexandra Zaninzhorov - One of the best experts on this subject based on the ideXlab platform.

  • heat shock protein 60 enhances cd4 cd25 regulatory t cell function via innate tlr2 signaling
    Journal of Clinical Investigation, 2006
    Co-Authors: Alexandra Zaninzhorov, Liora Cahalon, Raanan Margalit, Ofer Lider, Irun R. Cohen
    Abstract:

    CD4+CD25+ Tregs regulate immunity, but little is known about their own regulation. We now report that the human 60-kDa heat shock protein (HSP60) acts as a costimulator of human Tregs, both CD4+CD25int and CD4+CD25hi. Treatment of Tregs with HSP60, or its peptide p277, before anti-CD3 activation significantly enhanced the ability of relatively low concentrations of the Tregs to downregulate CD4+CD25– or CD8+ target T cells, detected as inhibition of target T cell proliferation and IFN-γ and TNF-α secretion. The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K, and p38, and were further enhanced by inhibition of ERK. HSP60-treated Tregs suppressed target T cells both by cell-to-cell contact and by secretion of TGF-β and IL-10. In addition, the expression of ERK, NF-κB, and T-bet by downregulated target T cells was inhibited. Thus, HSP60, a Self-Molecule, can downregulate adaptive immune responses by upregulating Tregs innately through TLR2 signaling.

  • heat shock protein 60 enhances cd4 cd25 regulatory t cell function via innate tlr2 signaling
    Journal of Clinical Investigation, 2006
    Co-Authors: Alexandra Zaninzhorov, Liora Cahalon, Raanan Margalit, Ofer Lider, Guy Tal, Irun R. Cohen
    Abstract:

    CD4+CD25+ Tregs regulate immunity, but little is known about their own regulation. We now report that the human 60-kDa heat shock protein (HSP60) acts as a costimulator of human Tregs, both CD4+CD25int and CD4+CD25hi. Treatment of Tregs with HSP60, or its peptide p277, before anti-CD3 activation significantly enhanced the ability of relatively low concentrations of the Tregs to downregulate CD4+CD25- or CD8+ target T cells, detected as inhibition of target T cell proliferation and IFN-gamma and TNF-alpha secretion. The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K, and p38, and were further enhanced by inhibition of ERK. HSP60-treated Tregs suppressed target T cells both by cell-to-cell contact and by secretion of TGF-beta and IL-10. In addition, the expression of ERK, NF-kappaB, and T-bet by downregulated target T cells was inhibited. Thus, HSP60, a Self-Molecule, can downregulate adaptive immune responses by upregulating Tregs innately through TLR2 signaling.

Liora Cahalon - One of the best experts on this subject based on the ideXlab platform.

  • heat shock protein 60 enhances cd4 cd25 regulatory t cell function via innate tlr2 signaling
    Journal of Clinical Investigation, 2006
    Co-Authors: Alexandra Zaninzhorov, Liora Cahalon, Raanan Margalit, Ofer Lider, Irun R. Cohen
    Abstract:

    CD4+CD25+ Tregs regulate immunity, but little is known about their own regulation. We now report that the human 60-kDa heat shock protein (HSP60) acts as a costimulator of human Tregs, both CD4+CD25int and CD4+CD25hi. Treatment of Tregs with HSP60, or its peptide p277, before anti-CD3 activation significantly enhanced the ability of relatively low concentrations of the Tregs to downregulate CD4+CD25– or CD8+ target T cells, detected as inhibition of target T cell proliferation and IFN-γ and TNF-α secretion. The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K, and p38, and were further enhanced by inhibition of ERK. HSP60-treated Tregs suppressed target T cells both by cell-to-cell contact and by secretion of TGF-β and IL-10. In addition, the expression of ERK, NF-κB, and T-bet by downregulated target T cells was inhibited. Thus, HSP60, a Self-Molecule, can downregulate adaptive immune responses by upregulating Tregs innately through TLR2 signaling.

  • heat shock protein 60 enhances cd4 cd25 regulatory t cell function via innate tlr2 signaling
    Journal of Clinical Investigation, 2006
    Co-Authors: Alexandra Zaninzhorov, Liora Cahalon, Raanan Margalit, Ofer Lider, Guy Tal, Irun R. Cohen
    Abstract:

    CD4+CD25+ Tregs regulate immunity, but little is known about their own regulation. We now report that the human 60-kDa heat shock protein (HSP60) acts as a costimulator of human Tregs, both CD4+CD25int and CD4+CD25hi. Treatment of Tregs with HSP60, or its peptide p277, before anti-CD3 activation significantly enhanced the ability of relatively low concentrations of the Tregs to downregulate CD4+CD25- or CD8+ target T cells, detected as inhibition of target T cell proliferation and IFN-gamma and TNF-alpha secretion. The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K, and p38, and were further enhanced by inhibition of ERK. HSP60-treated Tregs suppressed target T cells both by cell-to-cell contact and by secretion of TGF-beta and IL-10. In addition, the expression of ERK, NF-kappaB, and T-bet by downregulated target T cells was inhibited. Thus, HSP60, a Self-Molecule, can downregulate adaptive immune responses by upregulating Tregs innately through TLR2 signaling.

Raanan Margalit - One of the best experts on this subject based on the ideXlab platform.

  • heat shock protein 60 enhances cd4 cd25 regulatory t cell function via innate tlr2 signaling
    Journal of Clinical Investigation, 2006
    Co-Authors: Alexandra Zaninzhorov, Liora Cahalon, Raanan Margalit, Ofer Lider, Irun R. Cohen
    Abstract:

    CD4+CD25+ Tregs regulate immunity, but little is known about their own regulation. We now report that the human 60-kDa heat shock protein (HSP60) acts as a costimulator of human Tregs, both CD4+CD25int and CD4+CD25hi. Treatment of Tregs with HSP60, or its peptide p277, before anti-CD3 activation significantly enhanced the ability of relatively low concentrations of the Tregs to downregulate CD4+CD25– or CD8+ target T cells, detected as inhibition of target T cell proliferation and IFN-γ and TNF-α secretion. The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K, and p38, and were further enhanced by inhibition of ERK. HSP60-treated Tregs suppressed target T cells both by cell-to-cell contact and by secretion of TGF-β and IL-10. In addition, the expression of ERK, NF-κB, and T-bet by downregulated target T cells was inhibited. Thus, HSP60, a Self-Molecule, can downregulate adaptive immune responses by upregulating Tregs innately through TLR2 signaling.

  • heat shock protein 60 enhances cd4 cd25 regulatory t cell function via innate tlr2 signaling
    Journal of Clinical Investigation, 2006
    Co-Authors: Alexandra Zaninzhorov, Liora Cahalon, Raanan Margalit, Ofer Lider, Guy Tal, Irun R. Cohen
    Abstract:

    CD4+CD25+ Tregs regulate immunity, but little is known about their own regulation. We now report that the human 60-kDa heat shock protein (HSP60) acts as a costimulator of human Tregs, both CD4+CD25int and CD4+CD25hi. Treatment of Tregs with HSP60, or its peptide p277, before anti-CD3 activation significantly enhanced the ability of relatively low concentrations of the Tregs to downregulate CD4+CD25- or CD8+ target T cells, detected as inhibition of target T cell proliferation and IFN-gamma and TNF-alpha secretion. The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K, and p38, and were further enhanced by inhibition of ERK. HSP60-treated Tregs suppressed target T cells both by cell-to-cell contact and by secretion of TGF-beta and IL-10. In addition, the expression of ERK, NF-kappaB, and T-bet by downregulated target T cells was inhibited. Thus, HSP60, a Self-Molecule, can downregulate adaptive immune responses by upregulating Tregs innately through TLR2 signaling.

Ofer Lider - One of the best experts on this subject based on the ideXlab platform.

  • heat shock protein 60 enhances cd4 cd25 regulatory t cell function via innate tlr2 signaling
    Journal of Clinical Investigation, 2006
    Co-Authors: Alexandra Zaninzhorov, Liora Cahalon, Raanan Margalit, Ofer Lider, Irun R. Cohen
    Abstract:

    CD4+CD25+ Tregs regulate immunity, but little is known about their own regulation. We now report that the human 60-kDa heat shock protein (HSP60) acts as a costimulator of human Tregs, both CD4+CD25int and CD4+CD25hi. Treatment of Tregs with HSP60, or its peptide p277, before anti-CD3 activation significantly enhanced the ability of relatively low concentrations of the Tregs to downregulate CD4+CD25– or CD8+ target T cells, detected as inhibition of target T cell proliferation and IFN-γ and TNF-α secretion. The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K, and p38, and were further enhanced by inhibition of ERK. HSP60-treated Tregs suppressed target T cells both by cell-to-cell contact and by secretion of TGF-β and IL-10. In addition, the expression of ERK, NF-κB, and T-bet by downregulated target T cells was inhibited. Thus, HSP60, a Self-Molecule, can downregulate adaptive immune responses by upregulating Tregs innately through TLR2 signaling.

  • heat shock protein 60 enhances cd4 cd25 regulatory t cell function via innate tlr2 signaling
    Journal of Clinical Investigation, 2006
    Co-Authors: Alexandra Zaninzhorov, Liora Cahalon, Raanan Margalit, Ofer Lider, Guy Tal, Irun R. Cohen
    Abstract:

    CD4+CD25+ Tregs regulate immunity, but little is known about their own regulation. We now report that the human 60-kDa heat shock protein (HSP60) acts as a costimulator of human Tregs, both CD4+CD25int and CD4+CD25hi. Treatment of Tregs with HSP60, or its peptide p277, before anti-CD3 activation significantly enhanced the ability of relatively low concentrations of the Tregs to downregulate CD4+CD25- or CD8+ target T cells, detected as inhibition of target T cell proliferation and IFN-gamma and TNF-alpha secretion. The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K, and p38, and were further enhanced by inhibition of ERK. HSP60-treated Tregs suppressed target T cells both by cell-to-cell contact and by secretion of TGF-beta and IL-10. In addition, the expression of ERK, NF-kappaB, and T-bet by downregulated target T cells was inhibited. Thus, HSP60, a Self-Molecule, can downregulate adaptive immune responses by upregulating Tregs innately through TLR2 signaling.