Julia Roider

University Hospital München, München, Bavaria, Germany

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Publications (9)29.83 Total impact

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    ABSTRACT: Myeloid-derived suppressor cells (MDSC) are immature myeloid cells with immunosuppressive function. Compared to healthy controls(HC), no elevation of MDSC in chronic hepatitis-C(cHEP-C) was found, independent of genotype or viral load (p>0.25). Moreover, MDSC of cHEP-C inhibited CD8 T cell function as efficiently as MDSC of HC did. Since we detected neither quantitative nor qualitative differences to MDSC of HC we postulate that MDSC in peripheral blood are most likely not significant regarding immune-dysfunction in cHEP-C.
    Journal of Virology 04/2014; 88(13). DOI:10.1128/JVI.00113-14 · 4.65 Impact Factor
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    ABSTRACT: Methods for identifying physiologically relevant CD8 T cell epitopes are critically important not only for the development of T cell based vaccines but also for understanding host – pathogen interactions. As experimentally mapping an optimal CD8 T cell epitope is a tedious procedure, many bioinformatic tools have been developed that predict which peptides bind to a given MHC molecule. We assessed the ability of the CD8 T cell epitope prediction tools SYFPEITHI, CTLPred and IEDB to foretell nine experimentally mapped optimal HIV-specific epitopes.Randomly – for any of the subjects’ HLA type and with any matching score – the optimal epitope was predicted in 7/9 epitopes using SYFPEITHI, in 3/9 epitopes using CTLPred and in 9/9 epitopes using IEDB. The optimal epitope within the three highest ranks was given in 4/9 epitopes applying SYFPEITHI, in 2/9 epitopes applying CTLPred and in 7/9 epitopes applying IEDB when screening for all of the subjects’ HLA types. Knowing HLA restriction of the peptide of interest improved the ranking of the optimal epitope within the predicted results. Epitopes restricted by common HLA alleles were more likely to be predicted than those restricted by uncommon HLA alleles. Epitopes with aberrant lengths than the usual HLA-class I nonamers were most likely not predicted.Epitope prediction tools applied together with literature search for already described optimal epitopes narrow down possibilities of optimal epitopes within a screening peptide of interest. However, in our opinion the actual fine mapping of a CD8 T cell epitope cannot be replaced yet.This article is protected by copyright. All rights reserved.
    Immunology 04/2014; 143(2). DOI:10.1111/imm.12301 · 3.74 Impact Factor
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    ABSTRACT: Defining the optimal epitope of a CD8 T cell response towards a certain antigen is a multistep procedure that requires the performance of peptide truncation design, ELISPOT peptide titration assays, and assessing the HLA class I restriction of the defined epitope via intracellular cytokine staining assays with B cell lines and epitope-specific CD8 T cell lines.
    Methods in molecular biology (Clifton, N.J.) 01/2014; 1169:97-106. DOI:10.1007/978-1-4939-0882-0_10 · 1.29 Impact Factor
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    ABSTRACT: HIV evades CD8 T cell mediated pressure by viral escape mutations in targeted CD8 T cell epitopes. A viral escape mutation can lead to a decline of the respective CD8 T cell response. Our question was what happened after the decline of a CD8 T cell response and - in the case of viral escape - if a new CD8 T cell response towards the mutated antigen could be generated in a population not selected for certain HLA alleles. We studied 19 antiretroviral-naïve HIV-1 infected individuals with different disease courses longitudinally. A median number of 12 (range 2-24) CD8 T cell responses towards Gag and Nef were detected per study subject. A total of 30 declining CD8 T cell responses were studied in detail and viral sequence analyses showed amino acid changes in 25 (83%) of these. Peptide titration assays and definition of optimal CD8 T cell epitopes revealed 12 viral escape mutations with one de-novo response (8%). The de-novo response, however, showed less effector functions than the original CD8 T cell response. In addition we identified 4 shifts in immunodominance. For one further shift in immunodominance, the mutations occurred outside the optimal epitope and might represent processing changes. Interestingly, four adaptations to the virus (the de-novo response and 3 shifts in immunodominance) occurred in the group of chronically infected progressors. None of the subjects with adaptation to the changing virus carried the HLA alleles B57, B*58:01 or B27. Our results show that CD8 T cell responses adapt to the mutations of HIV. However it was limited to only 20% (5 out of 25) of the epitopes with viral sequence changes in a cohort not expressing protective HLA alleles.
    PLoS ONE 12/2013; 8(12):e80045. DOI:10.1371/journal.pone.0080045 · 3.53 Impact Factor
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    ABSTRACT: PURPOSE: To test a new assay based on an ex vivo cytokine release from whole blood for the monitoring of immune changes in human immunodeficiency virus (HIV)-infected patients. METHODS: A pilot study of outpatients with HIV infection (n = 9) at a large academic hospital who were divided into three groups: HIV-infected patients on highly active antiretroviral therapy (HAART) with a CD4(+) cell count >350/μL (group I) or a CD4(+) cell count <350/μL (group II) and HIV-infected HAART-naïve subjects with a CD4(+) cell count >350/μL (group III). All groups were compared with healthy volunteers (n = 3). The ex vivo cytokine release assay was performed in a three-step process: (1) blood collection, (2) whole-blood ex vivo incubation over 48 h without or with a standard set of well-defined recall antigens as comparable to those used formerly in the skin delayed-type hypersensitivity (DTH) test, (3) cytokine determination from the assay supernatant. RESULTS: Under stimulated conditions, untreated HIV-infected patients with a CD4(+) count >350/μL had similar interleukin-2 (IL-2) levels in the supernatant of the whole-blood incubation to HIV-infected patients on HAART with a low CD4(+) count. Both groups revealed lower IL-2 levels in the supernatant than HIV-infected patients on HAART and with a CD4(+) count >350/μL or healthy volunteers. The determination of interferon-γ and tumour necrosis factor-α in the supernatant showed a similar arrangement of cytokines between groups. CONCLUSIONS: Our results suggest that this cytokine release assay could be a suitable tool to mirror the immunological responsiveness of patients with HIV infection in a gradual manner; further studies are required in order to assess its value in HAART monitoring.
    Infection 03/2013; 41(3). DOI:10.1007/s15010-013-0445-8 · 2.86 Impact Factor
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    Retrovirology 09/2012; 9(2). DOI:10.1186/1742-4690-9-S2-P284 · 4.77 Impact Factor
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    ABSTRACT: Myeloid-derived suppressor cells (MDSCs) have been described as suppressors of T-cell functions in many tumor models. However, MDSC in HIV-1 infection have not been studied to date. As impaired T-cell function is a hallmark of chronic progressive HIV-1 infection, we hypothesized that MDSC also play a role here. Surface staining and flow cytometry analysis were performed on freshly isolated peripheral blood mononuclear cells (PBMC) of HIV-infected individuals and compared to healthy controls and individuals with lung carcinoma. MDSC of late-stage HIV-infected individuals were isolated using magnetic beads and cocultured with the respective CD8 T cells for evaluation of proliferative capacity. We found that chronically HIV-infected HAART-naive individuals had significantly higher CD11bCD14CD33CD15 MDSC levels than healthy controls (P = 0.01). MDSC frequencies showed a positive correlation with viral load (r = 0.24, P = 0.0002) and a negative correlation with CD4 cell count (r = 0.29, P < 0.0001). Initiation of HAART led to a rapid drop in MDSC levels. MDSC from HIV-infected progressors restricted the proliferative capacity of CD8 T cells from healthy donors and of Gag/Nef-specific CD8 T cells from HIV-controllers in vitro. Furthermore, CD11bCD14CD33CD15 MDSC induced the expansion of CD4CD25FoxP3 regulatory T cells when coincubated with PBMC from controllers in vitro. We conclude that chronic uncontrolled HIV-infection is associated with elevated levels of MDSC, which potentially contribute to the impaired T-cell responses characteristic for the progressive disease stage.
    AIDS (London, England) 04/2012; 26(12):F31-7. DOI:10.1097/QAD.0b013e328354b43f · 6.56 Impact Factor
  • Pneumologie 03/2012; 66(S 01). DOI:10.1055/s-0032-1302762
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    ABSTRACT: Antiretroviral treatment directed against HIV is highly effective, yet limited by drug resistance mutations. We hypothesized that CD8 T cells targeting drug-resistant HIV mutants are able to inhibit viral replication in the setting of a failing therapeutic regimen. We evaluated CD8 T-cell responses and mapped epitopes in HIV-infected patients by interferon-gamma Elispot and intracellular cytokine staining. Autologous virus was sequenced by RT-PCR. Viral replication inhibition assays were performed using M184V mutant virus and CD8 T cell lines. CD8 T-cell responses toward the regions of viral drug resistance mutations in Pol are frequent. Focusing on the M184V mutation, A*02:01-YQYVDDLYV and A*02:01-VIYQYVDDLYV were identified as optimal epitopes for the majority of study subjects. Viral replication of M184V HIV mutants was inhibited by CD8 T cell lines in vitro. In case of a failing lamivudine/emtricitabine containing regimen, individuals with a CD8 T-cell response toward M184V had a significant lower viral load than those without a CD8 response (p = 0.005). Two study subjects even achieved an undetectable viral load. Our data suggest that control of M184V mutant virus by CD8 T-cell responses is possible in vitro and in vivo. This control has important implications for therapeutic vaccination strategies.
    Medical Microbiology and Immunology 12/2011; 201(2):201-11. DOI:10.1007/s00430-011-0222-1 · 2.43 Impact Factor

Publication Stats

41 Citations
29.83 Total Impact Points


  • 2014
    • University Hospital München
      München, Bavaria, Germany
  • 2012–2014
    • Ludwig-Maximilian-University of Munich
      • • Department of Internal Medicine II
      • • Department of Internal Medicine IV
      München, Bavaria, Germany
    • Technische Universität München
      München, Bavaria, Germany