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Dive into the research topics where Fabienne Hadida is active.

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Featured researches published by Fabienne Hadida.


Cell | 1994

HIV AND T CELL EXPANSION IN SPLENIC WHITE PULPS IS ACCOMPANIED BY INFILTRATION OF HIV-SPECIFIC CYTOTOXIC T LYMPHOCYTES

Rémi Cheynier; Sven Henrichwark; Fabienne Hadida; Eric Pelletier; Eric Oksenhendler; Brigitte Autran; Simon Wain-Hobson

Human immunodeficiency virus (HIV) replication and T cell proliferation were investigated in situ by a PCR-based analysis of individual microdissected splenic white pulps. Founder effects, revealed by an exquisite compartmentalization of HIV genotypes and T cells, indicated the recruitment of latently infected CD4+ T cells through highly localized antigen presentation rather than the infection of CD4+ T lymphoblasts by blood-borne virus or immune complexes. HIV-infected white pulps could be infiltrated by HIV-specific cytotoxic T lymphocytes, thereby implicating them in CD4+ T cell destruction in vivo. Together these data describe an iterative and deleterious mechanism of antigen-driven T cell recruitment and activation, as well as HIV replication and spread, with consequent destruction of the newly infected cells.


Current Opinion in Immunology | 1996

Evolution and plasticity of CTL responses against HIV

B. Autran; Fabienne Hadida; Gaby Haas

Exceptionally potent cytotoxic T lymphocyte responses are generated after HIV invasion and probably control the primary infection as well as the asymptomatic phase of HIV infection. The chronic phase appears as a quasi-equilibrium between waves of new HIV variants and variant-specific CTLs, thus sustaining continuous CTL activation which eventually fails to eradicate HIV disease progression and the reascension of viral replication. Meanwhile, both the host and the virus develop various strategies either to stop or to evade this potentially deleterious permanent CTL activity. The transient effectiveness of CTLs opens perspectives for understanding disease progression generally as well as for immune therapeutic strategies.


Research in Virology | 1991

HIV-specific cytotoxic T lymphocytes against alveolar macrophages: specificities and downregulation.

B. Autran; Behazine Sadat-Sowti; Fabienne Hadida; A Parrot; Jean-Marcel Guillon; Fernando Plata; C Mayaud; Patrice Debré

To analyse the evolution of alveolar-lymphocyte-mediated cytotoxic activity directed against autologous alveolar macrophages (AM), cytotoxic assays against various HIV+ target cells were performed in a cohort of 75 patients with HIV-associated lymphoid interstitial pneumonitis (LIP) studied at distinct stages of HIV infection. Our data confirm that alveolar HIV-specific cytotoxic T lymphocytes (CTL) against AM were detectable before AIDS in patients with CD8+ LIP. Mild CD8+ lymphocytic alveolitis occurs silently in 62% of stage II and III patients with no respiratory symptoms. In these cases, the lack of spontaneous alveolar-lymphocyte-mediated cytotoxic activity against autologous AM may contrast with the detection of primary alveolar CTL specific for HIV proteins such as nef. In AIDS patients, the alveolar CTL lytic efficiency against both AM- and HIV-antigen-expressing cells can be inhibited by a suppressor factor produced by alveolar CD8+ CD57+ cells. Therefore, spontaneous CTL lysis of AM may be (1) limited to a subgroup of patients with active LIP and (2) controlled by distinct mechanisms, including suppressor phenomenons, and HIV replication levels in AM.


Immunology Letters | 1997

Dynamics of HIV variants and specific cytotoxic T-cell recognition in nonprogressors and progressors

Gaby Haas; Anne Hosmalin; Fabienne Hadida; Jörg Duntze; Patrice Debré; B. Autran

Infection with the human immunodeficiency virus (HIV) results in a disease characterized by a rapid viral replication, immunodeficiency and chronic immune activation. The vigorous polyspecific cytotoxic T-cell (CTL) response directed against multiple HIV epitopes reduces HIV-infected cell numbers, although unable to eradicate the virus. The plasticity of the specific CTL repertoire ensures adaptation to the high rate of viral variation that can be found in CTL epitopes of several HIV-1 proteins. However, viral persistence occurs despite continuous CTL recognition and although functional importance of conserved sites in the different HIV proteins may impose constraints to viral variation. In the reverse transcriptase (RT) which is a major target for antiretroviral therapy, the impact of the continuous pressure of drug therapy is more obvious than that of the CTLs. Shifts in immunodominant RT regions seem to allow the maintenance of the HIV-1 RT CTL recognition with disease progression and antiretroviral therapy. In respect to new highly active drug combinations, understanding the capacity of virus-specific CTLs to control residual viral variants seems very important and may allow development of efficient immunotherapies to prevent drug-induced viral resistance.


AIDS | 1991

MS-8209, a new amphotericin B derivative that inhibits HIV-1 replication in vitro and restores T-cell activation via the CD3/TcR in HIV-infected CD4+ cells

Daniel Cefai; Fabienne Hadida; Magdalena Jung; Patrice Debré; Jean-Gilles Vernin; Michel Seman

A new Amphotericin B derivative, MS-8209, which retains high antifungal activity with greatly reduced toxicity and improved solubility, has been developed. We investigated the antiviral properties of MS-8209 in Jurkat and CEM T-cell lines and in peripheral blood mononuclear cells infected in vitro with HIV-1BRU. Our results demonstrate, by determination of reverse transcriptase activity and p24 antigen level titration in cell culture supernatants, that MS-8209 inhibits HIV-1 replication in all cell types at concentrations without cytotoxicity. MS-8209 also prevents membrane expression of the HIV-1 large envelope glycoprotein gp120 and the decrease in CD4 level at the surface of infected cells. HIV-1-infected Jurkat cells exhibit a severe signalling defect at CD3 stimulation. Treatment with MS-8209 restores normal responsiveness at CD3 as assessed by measurement of inositol triphosphate accumulation and calcium flux. Finally, our results indicate that MS-8209 inhibits HIV-1BRU replication without preventing virus binding and penetration into target cells.


Human Gene Therapy | 1999

Acquired constitutive expression of interferon beta after gene transduction enhances human immunodeficiency virus type 1-specific cytotoxic T lymphocyte activity by a RANTES-dependent mechanism.

Fabienne Hadida; E. De Maeyer; Isabelle Cremer; B. Autran; Marco Baggiolini; Patrice Debré; V. Vieillard

CTL lines directed against HIV-1 antigens were generated from infected individuals and were transduced by the HMB-K(b)HuIFNbeta vector, resulting in low, constitutive expression of interferon beta (IFN-beta). The IFN-beta-transduced cells showed markedly increased HIV-1-specific, MHC class I-restricted CTL activity against HIV-1-LAI Gag, Pol, or Env antigens. This effect of IFN-beta was correlated with an overexpression of RANTES and completely abrogated by RANTES-blocking antibody. The present results provide the first evidence that IFN-beta transduction of CTL lines enhances HIV-specific cytotoxic activities through an upregulation of RANTES production. The efficient elimination of HIV-infected cells by IFN-beta-transduced CTL lines makes this gene therapy approach an attractive treatment for AIDS.


Advances in Experimental Medicine and Biology | 1995

Clonal Expansion of T Cells and HIV Genotypes in Microdissected Splenic White Pulps Indicates Viral Replication in Situ and Infiltration of HIV-Specific Cytotoxic T Lymphocytes

Rémi Cheynier; Sven Henrichwark; Fabienne Hadida; Eric Pelletier; Eric Oksenhendler; Brigitte Autran; Simon Wain-Hobson

Human immunodeficiency virus (HIV) replication and T cell proliferation was investigated in situ by a PCR based analysis of individual microdissected splenic white pulps. Founder effects, revealed by an exquisite compartmentalization of HIV genotypes and T cells, indicated the recruitment of latently infected CD4+ T cells through highly localized antigen presentation, rather than the infection of CD4+ T lymphoblasts by blood borne virus or immune complexes. HIV infected white pulps could be infiltrated by HIV specific cytotoxic T lymphocytes, so implicating them in CD4+ T cell destruction in vivo. Together these data describe an iterative and deleterious mechanism of antigen driven T cell recruitment and activation, HIV replication and spread, with consequent destruction of the newly infected cells.


European Journal of Immunology | 1991

A lectin-binding soluble factor released by CD8+CD57+ lymphocytes from AIDS patients inhibits T cell cytotoxicity

Behazine Sadat-Sowti; Patrice Debré; Jean-Marcel Guillon; Fabienne Hadida; B. Autran; Thierry Idziorek; Eric Okzenhendler; Christine Katlama; Mayaud C


Journal of Experimental Medicine | 1998

HIV-specific T cell cytotoxicity mediated by RANTES via the chemokine receptor CCR3.

Fabienne Hadida; Vincent Vieillard; Brigitte Autran; Ian Clark-Lewis; Marco Baggiolini; Patrice Debré


Journal of Immunology | 1999

Cutting Edge: RANTES Regulates Fas Ligand Expression and Killing by HIV-Specific CD8 Cytotoxic T Cells

Fabienne Hadida; Vincent Vieillard; Lucile Mollet; Ian Clark-Lewis; Marco Baggiolini; Patrice Debré

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Patrice Debré

Centre national de la recherche scientifique

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B. Autran

Centre national de la recherche scientifique

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Behazine Sadat-Sowti

Centre national de la recherche scientifique

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Gaby Haas

Centre national de la recherche scientifique

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Lucile Mollet

Centre national de la recherche scientifique

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Anne Hosmalin

Centre national de la recherche scientifique

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Jean-Marcel Guillon

Centre national de la recherche scientifique

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Jörg Duntze

Centre national de la recherche scientifique

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