The Experts below are selected from a list of 4395 Experts worldwide ranked by ideXlab platform
Annie Mirsoian - One of the best experts on this subject based on the ideXlab platform.
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out of sequence signal 3 paralyzes primary cd4 t cell dependent immunity
Immunity, 2015Co-Authors: Gail D Sckisel, Myriam N Bouchlaka, Arta M Monjazeb, Marka R Crittenden, Brendan D Curti, Danice E C Wilkins, Kory A Alderson, Can M Sungur, Erik Ames, Annie MirsoianAbstract:Primary T cell activation involves the integration of three distinct signals delivered in sequence: (1) antigen recognition, (2) costimulation, and (3) cytokine-mediated differentiation and expansion. Strong immunostimulatory events such as immunotherapy or infection induce profound cytokine release causing "bystander" T cell activation, thereby increasing the potential for autoreactivity and need for control. We show that during strong stimulation, a profound suppression of primary CD4(+) T-cell-mediated immune responses ensued and was observed across preclinical models and patients undergoing high-dose interleukin-2 (IL-2) therapy. This suppression targeted naive CD4(+) but not CD8(+) T cells and was mediated through Transient Suppressor of cytokine signaling-3 (SOCS3) inhibition of the STAT5b transcription factor signaling pathway. These events resulted in complete paralysis of primary CD4(+) T cell activation, affecting memory generation and induction of autoimmunity as well as impaired viral clearance. These data highlight the critical regulation of naive CD4(+) T cells during inflammatory conditions.
Gail D Sckisel - One of the best experts on this subject based on the ideXlab platform.
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out of sequence signal 3 paralyzes primary cd4 t cell dependent immunity
Immunity, 2015Co-Authors: Gail D Sckisel, Myriam N Bouchlaka, Arta M Monjazeb, Marka R Crittenden, Brendan D Curti, Danice E C Wilkins, Kory A Alderson, Can M Sungur, Erik Ames, Annie MirsoianAbstract:Primary T cell activation involves the integration of three distinct signals delivered in sequence: (1) antigen recognition, (2) costimulation, and (3) cytokine-mediated differentiation and expansion. Strong immunostimulatory events such as immunotherapy or infection induce profound cytokine release causing "bystander" T cell activation, thereby increasing the potential for autoreactivity and need for control. We show that during strong stimulation, a profound suppression of primary CD4(+) T-cell-mediated immune responses ensued and was observed across preclinical models and patients undergoing high-dose interleukin-2 (IL-2) therapy. This suppression targeted naive CD4(+) but not CD8(+) T cells and was mediated through Transient Suppressor of cytokine signaling-3 (SOCS3) inhibition of the STAT5b transcription factor signaling pathway. These events resulted in complete paralysis of primary CD4(+) T cell activation, affecting memory generation and induction of autoimmunity as well as impaired viral clearance. These data highlight the critical regulation of naive CD4(+) T cells during inflammatory conditions.
F C Lee - One of the best experts on this subject based on the ideXlab platform.
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single shot Transient Suppressor ssts for high current high slew rate microprocessor
Applied Power Electronics Conference, 1999Co-Authors: L Amoroso, M Donati, Xunwei Zhou, F C LeeAbstract:Future generation microprocessors are predicted to exhibit heavier loads and faster Transients. Conventional voltage regulator modules (VRM) need a large amount of output filter capacitors to meet future requirements and a huge number of decoupling capacitors, mainly due to the presence of parasitic inductance between the VRM and the microprocessor. In this paper, a new active damp concept is presented. By charging some auxiliary capacitors at higher voltage, it is possible to store the amount of charge required by the processor during the step up Transient; this extra charge can be locally delivered to the processor in a single shot manner, bypassing the slower VRM. In the same way, this circuit can sink the excess of charge that has to be removed during the step down Transient. By using this Transient Suppressor circuit, a conventional VRM can still provide adequate steady state regulation, while the size of decoupling and filter capacitors can be significantly reduced. Experimental results prove the validity of the concept.
Brendan D Curti - One of the best experts on this subject based on the ideXlab platform.
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out of sequence signal 3 paralyzes primary cd4 t cell dependent immunity
Immunity, 2015Co-Authors: Gail D Sckisel, Myriam N Bouchlaka, Arta M Monjazeb, Marka R Crittenden, Brendan D Curti, Danice E C Wilkins, Kory A Alderson, Can M Sungur, Erik Ames, Annie MirsoianAbstract:Primary T cell activation involves the integration of three distinct signals delivered in sequence: (1) antigen recognition, (2) costimulation, and (3) cytokine-mediated differentiation and expansion. Strong immunostimulatory events such as immunotherapy or infection induce profound cytokine release causing "bystander" T cell activation, thereby increasing the potential for autoreactivity and need for control. We show that during strong stimulation, a profound suppression of primary CD4(+) T-cell-mediated immune responses ensued and was observed across preclinical models and patients undergoing high-dose interleukin-2 (IL-2) therapy. This suppression targeted naive CD4(+) but not CD8(+) T cells and was mediated through Transient Suppressor of cytokine signaling-3 (SOCS3) inhibition of the STAT5b transcription factor signaling pathway. These events resulted in complete paralysis of primary CD4(+) T cell activation, affecting memory generation and induction of autoimmunity as well as impaired viral clearance. These data highlight the critical regulation of naive CD4(+) T cells during inflammatory conditions.
Erik Ames - One of the best experts on this subject based on the ideXlab platform.
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out of sequence signal 3 paralyzes primary cd4 t cell dependent immunity
Immunity, 2015Co-Authors: Gail D Sckisel, Myriam N Bouchlaka, Arta M Monjazeb, Marka R Crittenden, Brendan D Curti, Danice E C Wilkins, Kory A Alderson, Can M Sungur, Erik Ames, Annie MirsoianAbstract:Primary T cell activation involves the integration of three distinct signals delivered in sequence: (1) antigen recognition, (2) costimulation, and (3) cytokine-mediated differentiation and expansion. Strong immunostimulatory events such as immunotherapy or infection induce profound cytokine release causing "bystander" T cell activation, thereby increasing the potential for autoreactivity and need for control. We show that during strong stimulation, a profound suppression of primary CD4(+) T-cell-mediated immune responses ensued and was observed across preclinical models and patients undergoing high-dose interleukin-2 (IL-2) therapy. This suppression targeted naive CD4(+) but not CD8(+) T cells and was mediated through Transient Suppressor of cytokine signaling-3 (SOCS3) inhibition of the STAT5b transcription factor signaling pathway. These events resulted in complete paralysis of primary CD4(+) T cell activation, affecting memory generation and induction of autoimmunity as well as impaired viral clearance. These data highlight the critical regulation of naive CD4(+) T cells during inflammatory conditions.