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Boris Vargaftig

Researcher at Pasteur Institute

Publications -  15
Citations -  494

Boris Vargaftig is an academic researcher from Pasteur Institute. The author has contributed to research in topics: Ovalbumin & Eosinophil. The author has an hindex of 8, co-authored 15 publications receiving 489 citations.

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Evidence for platelet-activating factor as a mediator of endotoxin-induced gastrointestinal damage in the rat. Effects of three platelet-activating factor antagonists.

TL;DR: The potential role of platelet-activating factor (PAF) as a mediator of gastrointestinal ulceration associated with septic shock was examined in the rat.
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Dendritic cells recruited to the lung shortly after intranasal delivery of Mycobacterium bovis BCG drive the primary immune response towards a type 1 cytokine production

TL;DR: The results suggest that AM and particularly DC by secreting IL‐12 shortly after BCG delivery induce the long‐term persistence of IFN‐γ‐secreting T cells percolating in BCG‐loaded lung tissue.
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Platelets mediate the action of diethylcarbamazine on microfilariae

TL;DR: This report provides the first evidence that the effect of DEC is mediated by blood platelets with the additional triggering of a filarial excretory antigen (FEA), and the killing mechanism is antibody-independent and involves the participation of free radicals.
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Interactions between local inflammatory and systemic haematological effects of PAF-acether in the rat.

TL;DR: It is suggested that haemoconcentration, thrombocytopenia and leukocytosis are independent phenomena associated with the presence of PAF-acether in the bloodstream, these haematological changes and the local oedema induced by PAF -acether involve distinct mechanisms and the auto-inhibitory property of PAFs is not restricted to in vitro situations, but extends to local inflammation.
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Demonstration of the therapeutic potential of non-anaphylactogenic anti-IgE antibodies in murine models of skin reaction, lung function and inflammation.

TL;DR: Non-anaphylactogenic anti-IgE antibodies can markedly inhibit IgE levels and IgE-mediated allergic reactions, and since bronchoconstriction, BHR and lung eosinophilic inflammation can be suppressed, such antibodies may be attractive principles for the treatment of allergic asthma.