Alain Fischer
University of Paris
805 Papers
7.3K Citations
Alain Fischer is an academic researcher from University of Paris. The author has contributed to research in topics: Transplantation & Medicine. The author has an hindex of 143, co-authored 770 publications. Previous affiliations of Alain Fischer include French Institute of Health and Medical Research & Boston Children's Hospital.
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Papers
Long-term human T-helper lines producing specific helper factor reactive to influenza virus.
TL;DR: Both the cells and the high-potency antigen-specific helper factor which they produce act on human B cells in a genetically restricted manner, and preliminary mapping of the restriction indicates associations, but not identity, with HLA-DR.
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Loss of ARHGEF1 causes a human primary antibody deficiency
Amine Bouafia,Sébastien Lofek,Julie Bruneau,Loic Chentout,Hicham Lamrini,Amélie Trinquand,Marie-Céline Deau,Lucie Heurtier,Véronique Meignin,Capucine Picard,Elizabeth Macintyre,Olivier Alibeu,Marc Bras,Thierry Jo Molina,Marina Cavazzana,Isabelle André-Schmutz,Anne Durandy,Alain Fischer,Eric Oksenhendler,Sven Kracker +19 more
TL;DR: Results indicate that ARHGEF1 activity in human lymphocytes is involved in controlling actin cytoskeleton dynamics, restraining PI3K/AKT signaling, and confining B lymphocytes and myelocytes within their dedicated functional environment.
Heterogeneous telomere defects in patients with severe forms of dyskeratosis congenita
Fabien Touzot,Laetitia Gaillard,Laetitia Gaillard,Nadia Vasquez,Tangui Le Guen,Tangui Le Guen,Yves Bertrand,Jean Bourhis,Thierry Leblanc,Alain Fischer,Jean Soulier,Jean-Pierre de Villartay,Patrick Revy,Patrick Revy +13 more
TL;DR: Observations provide the notions that various telomere defects can lead to similar clinical features, andTelomere dysfunction in cells from patients with DC/HH is not always associated with short telomeres, and additional factors, likely involved in Telomere protection rather than in length regulation, are responsible for a subset of DC/ HH.
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Mutations in the adaptor-binding domain and associated linker region of p110δ cause Activated PI3K-δ Syndrome 1 (APDS1).
Lucie Heurtier,Hicham Lamrini,Loic Chentout,Marie-Céline Deau,Amine Bouafia,Jérémie Rosain,Jean-Marc Plaza,Mélanie Parisot,Benoit Dumont,Delphine Turpin,Etienne Merlin,Despina Moshous,Nathalie Aladjidi,Benedicte Neven,Capucine Picard,Marina Cavazzana,Alain Fischer,Anne Durandy,Jean-Louis Stephan,Sven Kracker +19 more
TL;DR: Three unrelated patients with novel heterozygous mutations in PIK3CD located in the ABD and the ABd-RBD linker region of p110δ as cause for APDS1 are reported, and two gain-of-function mutations thus affect domains not previously shown to be important in the increased p 110δ activity characteristic of this syndrome.
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Mouse macrophage development in the absence of the common gamma chain: defining receptor complexes responsible for IL-4 and IL-13 signaling.
TL;DR: It is concluded that signaling through the γc chain is not essential for the differentiation of mouse macrophage lineage, and IL‐4 up‐regulated major histocompatibility class II molecules and inhibited nitric oxide production from γ−c macrophages following stimulation with lipopolysaccharide and interferon‐γ.
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