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Philippe Saas

Researcher at French Institute of Health and Medical Research

Publications -  273
Citations -  9193

Philippe Saas is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Transplantation & Immune system. The author has an hindex of 45, co-authored 237 publications receiving 8111 citations. Previous affiliations of Philippe Saas include University of Burgundy & Geneva College.

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Human Leukocyte Antigen‐G5 Secretion by Human Mesenchymal Stem Cells Is Required to Suppress T Lymphocyte and Natural Killer Function and to Induce CD4+CD25highFOXP3+ Regulatory T Cells

TL;DR: It is reported that the nonclassic human leukocyte antigen (HLA) class I molecule HLA‐G is responsible for the immunomodulatory properties of MSCs and it is demonstrated that in addition to their action on the adaptive immune system, M SCs, through HLA•G5, affect innate immunity by inhibiting both NK cell‐mediated cytolysis and interferon‐γ secretion.
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Fas ligand expression by astrocytoma in vivo: maintaining immune privilege in the brain?

TL;DR: The findings suggest that FasL-induced apoptosis by astrocytoma cells may play a significant role in both immunosuppression and the regulation of tumor growth within the central nervous system.
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Role of Fas ligand (CD95L) in immune escape: the tumor cell strikes back

TL;DR: The potential interactions between tumor cells and the host immune response are thus more complex than previously thought; their elucidation will benefit the rational design of cancer immunotherapy strategies.
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Administration of herpes simplex–thymidine kinase–expressing donor T cells with a T-cell–depleted allogeneic marrow graft

TL;DR: Overall, the administration of low numbers of HS-tk-expressing T cells early following an HLA-identical BMT is associated with no acute toxicity, persistent circulation of the GMCs, and GCV-sensitive GVHD, and open the way to the infusion of higher numbers of gene-modified donor T cells to enhance post-BMT immune competence while preserving GCv-sensitive alloreactivity.
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CD3-specific antibody-induced immune tolerance involves transforming growth factor-beta from phagocytes digesting apoptotic T cells.

TL;DR: In this paper, the authors show that treatment of normal mice with intact antibody to CD3 increases systemic transforming growth factor-beta (TGF-beta) produced by phagocytes exposed to apoptotic T cells, which suggests that apoptosis is linked to active suppression in immune tolerance.