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Salem Chouaib

Researcher at Gulf Medical University

Publications -  338
Citations -  27323

Salem Chouaib is an academic researcher from Gulf Medical University. The author has contributed to research in topics: Cytotoxic T cell & Immune system. The author has an hindex of 70, co-authored 318 publications receiving 23414 citations. Previous affiliations of Salem Chouaib include Institut Gustave Roussy & Haukeland University Hospital.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

The host—tumor immune conflict: from immunosuppression to resistance and destruction

TL;DR: Evidence that, to escape the immune system, tumor cells not only produce immunosuppressive cytokines but also employ strategies involving altered susceptibility to tumor necrosis factor and Fas cytotoxic pathways and, in some circumstances, use of the Fas ligand to neutralize effector cells is discussed.
Journal Article

Prostaglandin E2 acts at two distinct pathways of T lymphocyte activation: inhibition of interleukin 2 production and down-regulation of transferrin receptor expression.

TL;DR: It is demonstrated that PGE2 exerts its inhibitory effects on T cell activation and proliferation via two distinct pathways: inhibition of IL 2 production and inhibition of transferrin receptor expression.