B Autran

Unité Inserm U1077, Caen, Lower Normandy, France

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Publications (332)1908.39 Total impact

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    ABSTRACT: Background Despite control of HIV infection under antiretroviral therapy (ART), immune T-cell activation persists in patients with controlled HIV infection, who are at higher risk of inflammatory diseases than the general population. PMNs play a key role in host defenses against invading microorganisms but also potentiate inflammatory reactions in cases of excessive or misdirected responses. Objective The aim of our study was to analyze PMN functions in 60 ART-treated and controlled HIV-infected patients (viral load, <20 RNA copies/mL; CD4 count, ≥350 cells/mm3) with (HIV[I] group) and without (HIV[NI] group) diseases related to an inflammatory process and to compare them with 22 healthy control subjects. Methods Flow cytometry was used to evaluate PMN functions in whole-blood conditions. We studied in parallel the activation markers of T lymphocytes and monocytes and the proinflammatory cytokine environment. Results Blood samples from HIV-infected patients revealed basal PMN hyperactivation associated with deregulation of the apoptosis/necrosis equilibrium. Interestingly, this hyperactivation was greater in HIV(I) than HIV(NI) patients and contrasted with a lack of monocyte activation in both groups. The percentage of circulating cells producing IL-17 was also significantly higher in HIV-infected patients than in control subjects and was positively correlated with markers of basal PMN activation. In addition, the detection of IL-22 overproduction in HIV(NI) patients suggests that it might contribute to counteracting chronic inflammatory processes during HIV infection. Conclusions This study thus demonstrates the presence of highly activated PMNs in HIV-infected patients receiving effective ART and the association of these cells with a specific IL-17/IL-22 environment.
    Journal of Allergy and Clinical Immunology 07/2014; · 12.05 Impact Factor
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    ABSTRACT: Cytomegalovirus (CMV) remains a leading cause of morbidity after solid organ transplantation. The efficiency of antivirals for the treatment of CMV infections may be hampered because of the emergence of CMV resistance to antivirals. The development of CMV multidrug-resistance, that remains uncommon but does occur, constitutes a clinically challenging complication and may contribute to difficult therapeutic management and adverse clinical outcome. We report here the observation of the emergence of a multidrug-resistant CMV infection in a heart-transplant recipient, and review the literature on similar cases to identify the potential strategies for the successful management of CMV multidrug-resistance among immunocompromised patients.
    Antiviral therapy 06/2014; · 3.07 Impact Factor
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    ABSTRACT: The magnitude, quality, and maintenance of immunological memory after infection or vaccination must be considered for future design of effective influenza vaccines. In 2009, the influenza pandemic produced disease that ranged from mild to severe, even fatal, illness in infected healthy adults and led to vaccination of a portion of the population with the adjuvanted, inactivated influenza A(H1N1)pdm09 vaccine. Here, we have proposed a multiparameter quantitative and qualitative approach to comparing adaptive immune memory to influenza 1 year after mild or severe infection or vaccination. One year after antigen encounter, severely ill subjects maintained high levels of humoral and polyfunctional effector/memory CD4+ T cells responses, while mildly ill and vaccinated subjects retained strong cellular immunity, as indicated by high levels of mucosal homing and degranulation markers on IFN-γ+ antigen-specific T cells. A principal component analysis distinguished 3 distinct clusters of individuals. The first group comprised vaccinated and mildly ill subjects, while clusters 2 and 3 included mainly infected individuals. Each cluster had immune memory profiles that differed in magnitude and quality. These data provide evidence that there are substantial similarities between the antiinfluenza response that mildly ill and vaccinated individuals develop and that this immune memory signature is different from that seen in severely ill individuals.
    The Journal of clinical investigation. 06/2014;
  • La Revue de Médecine Interne 06/2014; 35:A44. · 0.90 Impact Factor
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    ABSTRACT: Introduction – objectifs Exploration du réservoir dans les sous-populations CD4 circulantes (SP) après 2 ans d’un traitement antirétroviral initié en primoinfection VIH (PHI2). Matériels et méthodes 12 patients randomisés de l’essai OPTIPRIM. J0 et M24 : quantification de l’ADN-VIH total et analyse phylogénétique de la quasiespèce virale dans les cellules triées quiescentes, naïves (TN), mémoires centrales (TCM), transitionnelles (TTM), effectrices (TEM). M24 : capacité des SP à produire des virus par activation in vitro et comparaison des niveaux d’ADN-VIH dans les SP des PHI2 versus 9 patients traités en PHI 6 ans en médiane (PHI6) et 11 contrôleurs post-traitement traités en PHI (PTC). Résultats De J0 à M24 : augmentation du nombre des SP (p < 0,004), diminution du niveau d’ADN-VIH médian dans les PBMC de – 1,43 (p = 0,001), – 0,74 (TN), – 1,45 (TCM), – 1,48 (TTM), – 1,34 (TEM) (p < 0,004). Pas d’évolution de la diversité virale et production virale induite dans toutes les SP. Les TN et TCM étaient moins infectées que TTM et TEM (p < 0,009) et contribuaient moins au réservoir que les TTM (p = 0,019). Les niveaux d’ADN-VIH dans les SP des PHI2 étaient plus élevés que les faibles et similaires niveaux chez les PHI6 et PTC (p < 0,019). Un PHI2 maintien un statut de PTC 18 mois après arrêt du traitement avec des niveaux de réservoir, similaires à ceux des PTC. Conclusion Un traitement précoce de deux ans en PHI protège les TCM et TN de l’infection. Un traitement de plus longue durée est nécessaire pour atteindre une réduction profonde du réservoir VIH et augmenter les cas de PTC.
    Médecine et Maladies Infectieuses 06/2014; 44(6):9–10. · 0.75 Impact Factor
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    ABSTRACT: The aim of the study was to determine the molecular mechanisms underlying the quasi-equilibrium between HIV and its host in the model of functional cure represented by elite controllers who spontaneously maintain exceptionally low levels of HIV reservoirs. Whole-genome transcriptional study and quantification of the cell-associated HIV DNA and HIV RNA levels of the four major resting CD4 T-cell subsets in HIV-1-infected elite controllers, viremic long-term nonprogressors (vir-LTNPs), and uninfected individuals. We compared the whole-genome transcriptional profiles (ArrayExpress accession number E-MTAB-1480) of the four major resting CD4 T-cell subsets [naive (TN), central-memory (TCM), transitional-memory (TTM), and effector-memory (TEM)] from 14 HIV-1-infected individuals including seven elite controllers (E-LTNPs) and seven vir-LTNPs, and from seven uninfected individuals. The HIV-1 cellular DNA and mRNA levels were quantified in parallel in each sorted subset. Host gene transcriptomes followed subset differentiation and viremia except in E-LTNPs wherein TCM, the main CD4 cell compartment, showed the highest activity with three specific signatures involving overexpression of TCR and costimulation signaling pathways, overexpression of the PRDM-1/Blimp-1 transcriptional repressor, and downmodulation of type-I IFN-related genes. Among subsets, the PRDM1/Blimp-1 upregulation was associated with lower levels of both cellular HIV-DNA and HIV mRNA levels. This unique Blimp-1 transcriptional repressor signature and the contrast between host and virus transcriptional activities in TCM from elite controllers suggest Blimp-1 might be involved in controlling the HIV reservoirs in the key TCM subset.
    AIDS (London, England) 05/2014; · 4.91 Impact Factor
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    ABSTRACT: Rationale: The biology of fatal pandemic influenza infection remains undefined. Methods: This multicenter study included 34 unvaccinated patients with very severe or fatal confirmed influenza A(H1N1) infections. It analyzed plasma A(H1N1) 2009 RT-PCR, hemagglutinin 222G viral mutation, and humoral and cellular immune responses to the virus, assessed in hemagglutination inhibition (HI), microneutralization, ELISA, lymphoproliferative, ELISpot IFN-, and cytokine/chemokine assays. Measurements and Main Results: The patients' median age was 34 years. Influenza A(H1N1) 2009 viremia was detected in 4/34 cases, and a 222G hemagglutinin mutation in 7/17 cases, all of them with SOFA≥8. HI antibodies were detectable in 19/26 survivors and undetectable in all 6 fatal fulminant cases. ELISA and microneutralization titers were concordant. B-cell immunophenotyping and plasma levels of immunoglobulin classes did not differ between patients who survived and died. After immune complex dissociation, influenza ELISA serology became strongly positive in the bronchoalveolar lavage of the 2 fatal cases tested. H1N1-specific T-cell responses in lymphoproliferative and IFN- assays were weak in survivors' peripheral blood, and lymphoproliferative assays were negative in the 3 fatal cases tested. Plasma levels of IL-6 and IL-10 were high in fatal cases and correlated with severity. Finally, a negative HI serology 4 days after the onset of influenza symptoms predicted death from fulminant influenza (p=0.04). Conclusions: Early negative A(H1N1) 2009 HI serology can predict death from influenza. This negative serology in fatal cases in young adults reflects the trapping of anti-H1N1 antibodies in immune complexes in the lungs, associated with poor specific helper T-cell response.
    American Journal of Respiratory and Critical Care Medicine 03/2014; · 11.04 Impact Factor
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    ABSTRACT: Few studies have compared the impact of different antiretroviral regimens on residual immune activation and inflammation with discordant results. Aim of the study was to investigate the impact of various antiretroviral regimens on markers of immune activation and inflammation during the first two years of effective therapy. We studied HIV-infected antiretroviral-naive patients who began cART with either abacavir/lamivudine or tenofovir/emtricitabine, combined with ritonavir-boosted lopinavir (LPV/r), atazanavir (ATV/r) or efavirenz (EFV). All the patients had a virological response within 6 months, which was maintained for 2 years with no change in their ART regimen. C-reactive protein (hs-CRP), interleukin-6 (IL-6), soluble CD14 (sCD14), monokine induced by interferon-gamma (MIG) and interferon-gamma-inducible protein-10 (IP-10) were measured in stored plasma obtained at cART initiation and 24 months later. Mean changes from baseline were analyzed on loge-transformed values and multivariable linear regression models were used to study the effect of the treatment components, after adjusting for factors that might have influenced the choice of ART regimen or biomarker levels. Differences were expressed as the mean fold change percentage difference (Delta). Seventy-eight patients (91% males) with a median age of 43 years met the inclusion criteria. Their median baseline CD4 cell count was 315/mm3 and HIV-1 RNA level 4.6 log10 copies/ml. During the 2-years study period, IL-6, IP-10 and MIG levels fell significantly, while hs-CRP and sCD14 levels remained stable. IP-10 and MIG levels declined significantly less strongly with ATV/r than with EFV (IP-10Delta -57%, p = 0.011; MIGDelta -136%, p = 0.007), while no difference was noted between LPV/r and EFV. The decline in IL-6 did not differ significantly across the different treatment components. After the first 2 years of successful cART, IL-6, IP-10 and MIG fell markedly while hs-CRP and sCD14 levels remained stable. The only impact of ART regimen was a smaller fall in markers of immune activation with ATV/r than with EFV. Our results suggest that these markers could be worthwhile when evaluating new antiretroviral drugs.
    BMC Infectious Diseases 03/2014; 14(1):122. · 3.03 Impact Factor
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    ABSTRACT: Idiopathic CD4 T lymphocytopenia (ICL) is a rare and severe condition with limited available data. We conducted a French multicenter study to analyze the clinical and immunologic characteristics of a cohort of patients with ICL according to the Centers for Disease Control criteria.We recruited 40 patients (24 female) of mean age 44.2 ± 12.2 (19-70) years. Patients underwent T-lymphocyte phenotyping and lymphoproliferation assay at diagnosis, and experiments related to thymic function and interferon (IFN)-γ release by natural killer (NK) cell were performed. Mean follow-up was 6.9 ± 6.7 (0.14-24.3) years. Infectious, autoimmune, and neoplastic events were recorded, as were outcomes of interleukin 2 therapy.In all, 25 patients had opportunistic infections (12 with human papillomavirus infection), 14 had autoimmune symptoms, 5 had malignancies, and 8 had mild or no symptoms. At the time of diagnosis, the mean cell counts were as follows: mean CD4 cell count: 127/mm (range, 4-294); mean CD8: 236/mm (range, 1-1293); mean CD19: 113/mm (range, 3-547); and mean NK cell count: 122/mm (range, 5-416). Most patients had deficiency in CD8, CD19, and/or NK cells. Cytotoxic function of NK cells was normal, and patients with infections had a significantly lower NK cell count than those without (p = 0.01). Patients with autoimmune manifestations had increased CD8 T-cell count. Proliferation of thymic precursors, as assessed by T-cell rearrangement excision circles, was increased. Six patients died (15%). CD4 T-cell count <150/mm and NK cell count <100/mm were predictors of death.In conclusion, ICL is a heterogeneous disorder often associated with deficiencies in CD8, CD19, and/or NK cells. Long-term prognosis may be related to initial CD4 and NK cell deficiency.
    Medicine 03/2014; 93(2):61-72. · 4.35 Impact Factor
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    ABSTRACT: Although it is established that CD8 T-cell immunity is critical for the control of HIV replication in vivo, the key factors that determine antiviral efficacy are yet to be fully elucidated. Antigen-sensitivity and T-cell receptor (TCR) avidity have been identified as potential determinants of CD8 T-cell efficacy. However, there is no general consensus in this regard because the relationship between these parameters and the control of HIV infection has been established primarily in the context of immunodominant CD8 T-cell responses against the Gag263-272 KK10 epitope restricted by HLA-B27. To investigate the relationship between antigen-sensitivity, TCR avidity and HIV-suppressive capacity in vitro across epitope specificities and HLA class I restriction elements, we used a variety of techniques to study CD8 T-cell clones specific for Nef73-82 QK10 and Gag20-29 RY10, both restricted by HLA-A3, alongside CD8 T-cell clones specific for Gag263-272 KK10. For each targeted epitope, the linked parameters of antigen-sensitivity and TCR avidity correlated directly with antiviral efficacy. However, marked differences in HIV-suppressive capacity were observed between epitope specificities, HLA class I restriction elements and viral isolates. Collectively, these data emphasize the central role of the TCR as a determinant of CD8 T-cell efficacy and demonstrate that the complexities of antigen recognition across epitope and HLA class I boundaries can confound simple relationships between TCR engagement and HIV suppression.
    AIDS (London, England) 12/2013; · 4.91 Impact Factor
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    ABSTRACT: HIV reservoirs persistence despite antiretroviral therapy (ART) might be related to persistent immune activation and residual HIV production, requiring further therapeutic strategies. We demonstrated that the tyrosine kinase inhibitor (TKI) Dasatinib, used for chronic myeloid leukaemia, significantly blocks in vitro HIV1 production by 3.4 logs in HIV1-infected primary CD4 T lymphocytes, by inhibiting cell activation and proliferation, without cell toxicity. This molecule deserves to be investigated further for HIV cure strategies to hinder persistent immune activation and residual viral production.
    AIDS (London, England) 12/2013; · 4.91 Impact Factor
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    ABSTRACT: The present study evaluated immunogenicity and tolerance of two-dose influenza A/H1N1pdm09 vaccination in allogeneic hematopoietic stem cell transplantation (HSCT) recipients, and compared the vaccine-induced humoral response to that triggered by natural infection in another group of HSCT patients. Adult allogeneic HSCT recipients vaccinated with two doses of influenza A/H1N1pdm09 vaccine, separated by 3 weeks, and patients with proven influenza A/H1N1pdm09 infection were included. Antibody responses were measured by hemagglutination-inhibition assay (1) on days 0, 21, 42 and 6 months after the first vaccine injection in vaccinated patients and (2) before pandemic and after influenza A/H1N1pdm09 infection, in patients presented natural infection. At baseline, 3% of 59 recipients of adjuvanted vaccine and 0% of 20 infected patients were seroprotected (antibody titer≥1/40). Seroprotection rate observed 42 days after vaccination was not different from that observed after natural infection (66% and 60% respectively, p=0.78). In vaccinated patients, seroprotection rate increased significantly from 54% to 66% between day 21 and 42 (p=0.015). Moreover, after 6 months, seroprotection rate in 21 vaccinated patients was similar to that observed in 10 infected patients evaluated at least 76 days after infection (D76-217) (60% and 81% respectively, p=0.2). In multivariate analysis, no immunosuppressive treatment or chronic graft-versus-host disease (GVHD) and longer time between transplantation and vaccination/infection were associated with a stronger humoral response. The adjuvanted vaccine was safe with low rate of GVHD worsening. In HSCT recipients, two doses of influenza A/H1N1pdm09 adjuvanted vaccine were safe and induced a humoral response comparable to that triggered by natural infection in these patients.
    Vaccine 12/2013; · 3.77 Impact Factor
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    ABSTRACT: The relevance of low-level HIV DNA in patients who have undergone prolonged therapy is not well understood. The objective of this study was to determine factors that influence the establishment of low-level HIV DNA in long-term treated patients (excluding treatment since acute infection). This was a cross-sectional study involving 243 patients receiving highly active antiretroviral therapy (HAART) for ≥6 months (median: 9 years of treatment) with plasma HIV RNA <50 copies/mL at the study timepoint, for whom total DNA measurements were performed. Patients treated since early acute infection or receiving cancer chemotherapeutic/immunosuppressive agents were excluded from the study. Overall, the median HIV DNA was 372 copies/10(6) peripheral blood mononuclear cells (PBMCs). Forty-seven patients had levels of HIV DNA below the limit of detection and 58 patients had low-level HIV DNA (<100 copies/10(6) PBMCs). In multivariate analysis, a low total HIV DNA in HAART-treated patients was clearly associated with a low HIV RNA pre-therapeutic viral load (P < 0.0001), regardless of the cut-off used. These results may be helpful to identify candidates for future trials aiming at a functional cure of HIV infection, since low total HIV DNA levels will most likely be a prerequisite of successful immunological control of HIV replication.
    Journal of Antimicrobial Chemotherapy 11/2013; · 5.34 Impact Factor
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    ABSTRACT: We have developed a novel immunotherapeutic vaccine (VAC-3S), comprised of 3S peptide, a highly conserved HIV gp41motif coupled to commercially used carrier and adjuvant. The 3S motif leads, by NKp44L expression on CD4+ T cells (CD4), to apoptosis of uninfected CD4 (Figure 1 below). In vitro, anti-3S antibodies (Ab) protect CD4 from apoptosis. In cohort studies, anti-3S Ab correlate with lack of CD4 decrease and/or disease progression. VAC-3S primate proof-of-concept showed effect on immune and inflammatory biomarkers [selected data shown below]. Dose ranging studies, GLP toxicity and local tolerance studies were performed in rats/mice and rats, respectively.  Prospective, randomized, placebo-controlled, double-blind dose-escalation study designed to assess safety and immunogenicity of 0.1, 1, 10 µg of 3S antigen present in VAC-3S with 3 IM immunizations at Day0, W4, W8, and a fourth immunization at W32 for the 1 and 10 µg arms [Figure 2].  Primary objective : safety & tolerability  Secondary objectives : immunogenicity, plasma anti-3S Ab titers, NKp44L expression on CD4 + T cells, CD4 + , CD8 + T cell count and percentages, CD4/CD8 ratio, expression of markers of lymphocyte activation (CD25, CD38, HLA-DR) on CD45 + CD3 + CD4 + , CD45 + CD3 + CD8 + and CD45 + CD3 -CD8 + cells, expression of markers of
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    ABSTRACT: We have developed a novel immunotherapeutic vaccine (VAC-3S), comprised of 3S peptide, a highly conserved HIV gp41motif coupled to commercially used carrier and adjuvant. The 3S motif leads, by NKp44L expression on CD4+ T cells (CD4), to apoptosis of uninfected CD4 (Figure 1 below). In vitro, anti-3S antibodies (Ab) protect CD4 from apoptosis. In cohort studies, anti-3S Ab correlate with lack of CD4 decrease and/or disease progression. VAC-3S primate proof-of-concept showed effect on immune and inflammatory biomarkers [selected data shown below]. Dose ranging studies, GLP toxicity and local tolerance studies were performed in rats/mice and rats, respectively.  Prospective, randomized, placebo-controlled, double-blind dose-escalation study designed to assess safety and immunogenicity of 0.1, 1, 10 µg of 3S antigen present in VAC-3S with 3 IM immunizations at Day0, W4, W8, and a fourth immunization at W32 for the 1 and 10 µg arms [Figure 2].  Primary objective : safety & tolerability  Secondary objectives : immunogenicity, plasma anti-3S Ab titers, NKp44L expression on CD4 + T cells, CD4 + , CD8 + T cell count and percentages, CD4/CD8 ratio, expression of markers of lymphocyte activation (CD25, CD38, HLA-DR) on CD45 + CD3 + CD4 + , CD45 + CD3 + CD8 + and CD45 + CD3 -CD8 + cells, expression of markers of
    AIDS Research and Human Retroviruses., AIDS Vaccine Conference, Barcelona, Spain; 10/2013
  • Blood 09/2013; 122(13):2282-3. · 9.78 Impact Factor
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  • Guislaine Carcelain, Brigitte Autran
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    ABSTRACT: Immune-based therapy (IBT) interventions have found a window of opportunity within some limitations of the otherwise successful combined antiretroviral therapy (cART). Two major paradigms drove immunotherapeutic research to combat human immunodeficiency virus (HIV) infection. First, IBTs were proposed either to help restore CD4(+) T-cell counts in cases of therapeutic failures with cytokines, interleukin-2 (IL-2) or IL-7, or to better control HIV and disease progression during treatment interruptions with anti-HIV therapeutic candidate vaccines. The most widely used candidates were HIV-recombinant live vector-based alone or combined with other vaccine compounds and dendritic cell (DC) therapies. A more recent and current paradigm aims at achieving HIV cure by combining IBT with cART using either cytokines to reactivate virus production in latently infected cells and/or therapeutic immunization to boost HIV-specific immunity in a 'shock and kill' strategy. This review summarizes the rationale, hopes, and mechanisms of successes and failures of these cytokine-based and vaccine-based immune interventions. Results from these first series of IBTs have been so far somewhat disappointing in terms of clinical relevance, but have provided lessons that are discussed in light of the future combined strategies to be developed toward an HIV cure.
    Immunological Reviews 07/2013; 254(1):355-71. · 12.16 Impact Factor
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    ABSTRACT: γδ T cells represent a subset of unconventional T lymphocytes that are known for their reactivity against different pathogens and considered as intermediate mediators between adaptive and innate immunity. We provide in this paper further insights underlying the changes that affect the γδ T cell compartment with advanced age in humans. We show that both aging and CMV infection impact independently on the γδ T cell compartment. Most γδ T cells are significantly affected by age and present a decreased frequency in the elderly. The decline of the γδ T cell pool appears to be independent from the activity of the thymus, arguing in favor of an extrathymic site of γδ T cell production in humans. Of note, CMV infection, which is directly associated with the activation of the pool of Vδ2(-) γδ T cells, promotes nonetheless the inflation of this compartment throughout life. CMV seropositivity accentuates further the accumulation of highly differentiated lymphocytes in Vδ2(-) γδ T cell subsets with time, in contrast to Vδ2(+) γδ T cells, which maintain a less differentiated phenotype. This is similar to the effect of CMV on αβ T cells and suggests that γδ T cells may vary in differentiation phenotype according to distinct stimuli or pathogens.
    The Journal of Immunology 07/2013; · 5.52 Impact Factor

Publication Stats

9k Citations
1,908.39 Total Impact Points

Institutions

  • 2001–2014
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 2010–2013
    • Polytech Paris-UPMC
      Lutetia Parisorum, Île-de-France, France
    • Centre Hospitalier Gabriel Martin
      Lutetia Parisorum, Île-de-France, France
  • 2004–2013
    • Pierre and Marie Curie University - Paris 6
      • Unité immunité et infection
      Paris, Ile-de-France, France
  • 2011
    • Université Victor Segalen Bordeaux 2
      Burdeos, Aquitaine, France
  • 2006–2011
    • University of Tours
      Tours, Centre, France
  • 1998–2011
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
    • Hôpital Paul-Brousse – Hôpitaux universitaires Paris-Sud
      Île-de-France, France
    • Max Planck Institute for Infection Biology
      • Department of Molecular Biology
      Berlin, Land Berlin, Germany
  • 1987–2009
    • Hôpital La Pitié Salpêtrière (Groupe Hospitalier "La Pitié Salpêtrière - Charles Foix")
      • • Service d’Hépato - Gastro - Entérologie
      • • Service de Médecine Interne 1
      Lutetia Parisorum, Île-de-France, France
  • 2008
    • Assistance Publique – Hôpitaux de Paris
      Lutetia Parisorum, Île-de-France, France
  • 2004–2008
    • Université Paris-Sud 11
      Orsay, Île-de-France, France
  • 2000
    • Institut Curie
      Lutetia Parisorum, Île-de-France, France
  • 1996–2000
    • French National Centre for Scientific Research
      Lutetia Parisorum, Île-de-France, France
  • 1997
    • Hôpital Foch
      Lutetia Parisorum, Île-de-France, France
  • 1995
    • Hôpitaux Universitaires La Pitié salpêtrière - Charles Foix
      Lutetia Parisorum, Île-de-France, France
  • 1994
    • Institut Pasteur de Lille
      Lille, Nord-Pas-de-Calais, France
  • 1992
    • Institut Universitaire de France
      Lutetia Parisorum, Île-de-France, France
  • 1989–1990
    • University of Pécs
      • Institute of Medical Microbiology and Immunology
      Pécs, Baranya megye, Hungary