M
Maan El-Khatib
Researcher at Boston University
Publications - 7
Citations - 1669
Maan El-Khatib is an academic researcher from Boston University. The author has contributed to research in topics: Cytotoxic T cell & Fas ligand. The author has an hindex of 7, co-authored 7 publications receiving 1662 citations. Previous affiliations of Maan El-Khatib include Boston Medical Center.
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Journal ArticleDOI
Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation
Shyr-Te Ju,David J. Panka,Haili Cui,Rachel Ettinger,Maan El-Khatib,David H. Sherr,Ben Z. Stanger,Ann Marshak-Rothstein +7 more
TL;DR: It is shown that receptor crosslinking induces Fas ligand and upregulates Fas, and that the ensuing engagement of Fas by Fasligand activates the cell-death programme.
Journal ArticleDOI
Fas (CD95)/Fas ligand interactions regulate antigen-specific, major histocompatibility complex-restricted T/B cell proliferative responses.
Metin Ozdemirli,Maan El-Khatib,Linda C. Foote,Julia K. M. Wang,Ann Marshak-Rothstein,Thomas L. Rothstein,Shyr-Te Ju +6 more
TL;DR: The results demonstrate that FasL cytotoxicity is a negative regulatory mechanism for both T and B cell proliferative responses and that Fas‐Ig can be an immunopotentiating agent for both B and T cell immunity.
Journal Article
The cytotoxic process of CD4 Th1 clones.
TL;DR: The data demonstrate that the cytotoxic process of Th1 clones uses an activation-dependent cytot toxic machinery to deliver a short-lived, short-ranged, and quick-acting lethal hit to target, which induces a program in target for DNA fragmentation.
Journal ArticleDOI
Regulation of T-Cell Death Genes: Selective Inhibition of FasL- but Not Fas-Mediated Function
Haili Cui,David H. Sherr,Maan El-Khatib,Ken Matsui,David J. Panka,Ann Marshak-Rothstein,Shyr-Te Ju +6 more
TL;DR: It is demonstrated that FasL gene activation, but not Fas up-regulation, is critical for AICD and that Dex and all-trans RA selectively inhibits FasL butNot Fas function and the system may prove useful for the identification of critical factors regulating T-cell death genes.
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The molecular mechanism of FasL-mediated cytotoxicity by CD4+ Th1 clones.
TL;DR: This study provides the first molecular view in terms of FasL/Fas of the cytotoxic process of CD+ Th1 cells and demonstrates that FasL-mediated lethal hit is critically dependent on conjugate formation and, once delivered, the effector-independent target lysis proceeds.