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Yeste, Ada

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Yeste

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Ada

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Yeste, Ada

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2014 - 20162

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Author's Publications: search.filters.isAuthorOfPublication.373f4b56-23b8-46a3-9ffc-5a31524378e9

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    IL-21 induces IL-22 production in CD4+ T-cells
    (2014) Yeste, Ada; Mascanfroni, Ivan D.; Nadeau, Meghan; Burns, Evan J.; Tukpah, Ann-Marcia; Santiago, Andrezza; Wu, Chuan; Patel, Bonny; Kumar, Deepak; Quintana, Francisco
    IL-22 produced by innate lymphoid cells (ILCs) and CD4+ T cells plays an important role in host defense and mucosal homeostasis, thus it is important to investigate the mechanisms that regulate IL-22 production. We investigated the regulation IL-22 production by CD4+ T cells. Here we show that IL-21 triggers IL-22, but not IL-17 production by CD4+ T cells. STAT3, activated by IL-21, controls the epigenetic status of the il22 promoter and its interaction with the aryl hydrocarbon receptor (AhR). Moreover, IL-21 and AhR signaling in T cells control IL-22 production and the development of dextran sodium sulfate-induced colitis in ILC-deficient mice. Thus, we have identified IL-21 as an inducer of IL-22 production in CD4+ T cells in vitro and in vivo.
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    Serum lipid antibodies are associated with cerebral tissue damage in multiple sclerosis
    (Ovid Technologies (Wolters Kluwer Health), 2016) Bakshi, Rohit; Yeste, Ada; Patel, B.; Tauhid, Shahamat; Tummala, Subhash; Rahbari, R.; Chu, Renxin; Regev, Keren; Kivisakk, Pia; Weiner, Howard; Quintana, Francisco
    Objective: To determine whether peripheral immune responses as measured by serum antigen arrays are linked to cerebral MRI measures of disease severity in multiple sclerosis (MS). Methods: In this cross-sectional study, serum samples were obtained from patients with relapsing-remitting MS (n = 21) and assayed using antigen arrays that contained 420 antigens including CNS-related autoantigens, lipids, and heat shock proteins. Normalized compartment-specific global brain volumes were obtained from 3-tesla MRI as surrogates of atrophy, including gray matter fraction (GMF), white matter fraction (WMF), and total brain parenchymal fraction (BPF). Total brain T2 hyperintense lesion volume (T2LV) was quantified from fluid-attenuated inversion recovery images. Results: We found serum antibody patterns uniquely correlated with BPF, GMF, WMF, and T2LV. Furthermore, we identified immune signatures linked to MRI markers of neurodegeneration (BPF, GMF, WMF) that differentiated those linked to T2LV. Each MRI measure was correlated with a specific set of antibodies. Strikingly, immunoglobulin G (IgG) antibodies to lipids were linked to brain MRI measures. Based on the association between IgG antibody reactivity and each unique MRI measure, we developed a lipid index. This comprised the reactivity directed against all of the lipids associated with each specific MRI measure. We validated these findings in an additional independent set of patients with MS (n = 14) and detected a similar trend for the correlations between BPF, GMF, and T2LV vs their respective lipid indexes. Conclusions: We propose serum antibody repertoires that are associated with MRI measures of cerebral MS involvement. Such antibodies may serve as biomarkers for monitoring disease pathology and progression.