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• W3199986095 abstract "Naive uncommitted CD4+ T lymphocytes can becomeeffector T helper cells by signals derived from the T cell receptor(TCR) and the cytokine milieu. Each T helper subset has distinctfunctional and phenotypical characteristics and can determine theimmune response against pathogens. The Th1 subset is characterizedby the production of IL-2 and IFN-γ and is involved incell-mediated inflammatory responses. The Th2 subset ischaracterized by the production of IL-4 and functionally, theycombat extracellular pathogens, enhance antibody production and theresponse from innate immune cells. The mechanisms by which the CD4+T cells differentiate into these polarized groups are not wellunderstood. A number of studies suggest that upon T cellactivation, actin-dependent signaling may be important for theintracellular signaling cascades leading to effector T celldevelopment. The Wiskott-Aldrich Syndrome protein (WASp), throughits role as a key regulator of the actin cytoskeleton, has beensuggested to be the link between actin cytoskeleton movement andtranscriptional activation of cells. Defects associated with thisprotein cause the Wiskott-Aldrich Syndrome (WAS) in humans;characterized by the triad of thrombocytopenia, skin disorders andimmune deficiencies. Studies investigating the role of the actincytoskeleton through WASp highlighted the essential role for theactin cytoskeleton in basic T cell functions. Given the essentialroles of the actin cytoskeleton in T cell functions and the knowndefective pathogen clearance in human WAS patients, we investigatedthe role of WASp in CD4+ T cell immune responses. We investigatedthe role for WASp in mediating Th1 effector function in vitro,through the delivery of signals from the TCR. We found WASp is anessential component of the CD4+ T cells secretory pathway.WASp-deficient T cells failed to polarize the secretory machinerytoward a target cell and showed an unexpected and striking block incytokine, but not chemokine, secretion. To investigate if WASpplays a redundant role in effector cytokine release, we testedWASp-deficient T cell effector function in an APC-dependent system.Surprisingly, signals other that the TCR, provided by wild typeAPCs enable WASp-deficient CD4+ T cells to release Th1 cytokines.Our studies suggested interactions between LFA-1 and ICAMfacilitate effector cytokine release in the absence of WASp. WASpplays a critical role in Th2 effector function. We demonstratedsignals for early events leading to the induction of the Th2program are WASp-independent. However, signals required for theproduction of effector IL-4 cytokine are defective in the absenceof WASp, despite normal levels of IL-4 cytokine gene mRNAupregulation. Thus in the absence of WASp there was a strikinguncoupling of cytokine transcription and protein production. Ourstudies demonstrated WASp plays a non-redundant role in Th2, butnot Th1, effector function. The significance of WASp in T helpercell differentiation in vivo remains unclear. We investigated therole of WASp…" @default.
• W3199986095 created "2021-09-27" @default.
• W3199986095 creator A5064310124 @default.
• W3199986095 date "2009-01-01" @default.
• W3199986095 modified "2023-09-24" @default.
• W3199986095 title "The Role of the Wiskott-Aldrich Syndrome protein (WASp)in T helper cell differentiation and effector function" @default.
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