Abdallah Badou

Prof. Abdallah Badou

orcid
avatar
Co-authors
avatar
Following
avatar
Followers

Research Focus & Metrics

Explore full metrics on Scilit

Academic Career Length

30Years (1997-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
1 November 2007 in Hepatology
Verified
Journal Article
Open access
PDF file
AWAzuma Watanabe
Azuma Watanabe
AHArdeshir Hashmi
Ardeshir Hashmi
DGDawidson Gomes
Dawidson Gomes
TTTerrence Town
Terrence Town
ABAbdallah Badou
Abdallah Badou
WMWajahat Zafar Mehal
Wajahat Zafar Mehal
Apoptosis of hepatocytes results in the development of liver fibrosis, but the molecular signals mediating this are poorly understood. Degradation and modification of nuclear DNA is a central feature of apoptosis, and DNA from apoptotic mammalian cells is known to activate immune cells via Toll-like receptor 9 (TLR9). We tested if DNA from apoptotic hepatocytes can induce hepatic stellate cell (HSC) differentiation. Our data show that apoptotic hepatocyte DNA and cytidine-phosphate-guanosine oligonucleotides induced up-regulation of transforming growth factor β1 and collagen 1 messenger RNA both in the human HSC line LX-2 and in primary mouse HSCs. These effects were opposed by TLR9 antagonists. We have recently shown that adenosine inhibits HSC chemotaxis, and we now show that apoptotic hepatocyte DNA also inhibits platelet-derived growth factor (PDGF)-mediated HSC chemotaxis. Inhibition of HSC chemotaxis by PDGF was blocked by TLR9 antagonists, and was absent in primary HSCs from mice deficient in TLR9 or the TLR adaptor molecule MyD88. Stimulation of TLR9 on HSCs blocked signaling by the PDGF signaling molecule inositol 1,4,5-triphosphate and reduced PDGF-mediated increase in cytosolic Ca2+. Conclusion: DNA from apoptotic hepatocytes acts as an important mediator of HSC differentiation by (1) providing a stop signal to mobile HSCs when they have reached an area of apoptosing hepatocytes and (2) inducing a stationary phenotype-associated up-regulation of collagen production.
2 November 2018 in Journal of Leukocyte Biology
Verified
Journal Article
Closed access
PDF file
DCDounia Chraa
Dounia Chraa
ANAsmaa Naim
Asmaa Naim
DODaniel Olive
Daniel Olive
ABAbdallah Badou
Abdallah Badou
9 July 2021 in Frontiers in Immunology
Verified
Journal Article
Open access
PDF file
AGAmina Ghouzlani
Amina Ghouzlani
SKSarah Kandoussi
Sarah Kandoussi
MTMariam Tall
Mariam Tall
KRKonala Priyanka Reddy
Konala Priyanka Reddy
SRSoumaya RAFII
Soumaya RAFII
ABAbdallah Badou
Abdallah Badou
Gliomas are the most common primary brain tumors in adults. Despite the fact that they are relatively rare, they cause significant morbidity and mortality. High-grade gliomas or glioblastomas are rapidly progressing tumors with a very poor prognosis. The presence of an intrinsic immune system in the central nervous system is now more accepted. During the last decade, there has been no major progress in glioma therapy. The lack of effective treatment for gliomas can be explained by the strategies that cancer cells use to escape the immune system. This being said, immunotherapy, which involves blockade of immune checkpoint inhibitors, has improved patients’ survival in different cancer types. This novel cancer therapy appears to be one of the most promising approaches. In the present study, we will start with a review of the general concept of immune response within the brain and glioma microenvironment. Then, we will try to decipher the role of various immune checkpoint inhibitors within the glioma microenvironment. Finally, we will discuss some promising therapeutic pathways, including immune checkpoint blockade and the body’s effective anti-glioma immune response.
19 May 1997 in Journal of Experimental Medicine
Verified
Journal Article
Open access
PDF file
FBFrank Bridoux
Frank Bridoux
ABAbdallah Badou
Abdallah Badou
Abdelhadi SaoudiAbdelhadi Saoudi
Abdelhadi Saoudi
IBIsabelle Bernard
Isabelle Bernard
EDElvira Druet
Elvira Druet
LPLucette Pelletier
Lucette Pelletier
Autoreactive anti–MHC class II T cells are found in Brown Norway (BN) and Lewis (LEW) rats that receive either HgCl2 or gold salts. These T cells have a T helper cell 2 (Th2) phenotype in the former strain and are responsible for Th2-mediated autoimmunity. In contrast, T cells that expand in LEW rats produce IL-2 and prevent experimental autoimmune encephalomyelitis, a cell-mediated autoimmune disease. The aim of this work was to investigate, using T cell lines derived from HgCl2-injected LEW rats (LEWHg), the effect of these autoreactive T cells on the development of Th2-mediated autoimmunity. The five LEWHg T cell lines obtained protect against Th2-mediated autoimmunity induced by HgCl2 in (LEW × BN)F1 hybrids. The lines produce, in addition to IL-2, IFN-γ and TGF-β, and the protective effect is TGF-β dependent since protection is abrogated by anti-TGF-β treatment. These results identify regulatory, TGF-β–producing, autoreactive T cells that are distinct from classical Th1 or Th2 and inhibit both Th1- and Th2-mediated autoimmune diseases.
1 January 2008 in Immunity
Verified
Journal Article
Closed access
DMDidi Matza
Didi Matza
ABAbdallah Badou
Abdallah Badou
KKKoichi S. Kobayashi
Koichi S. Kobayashi
KGKaren Goldsmith-Pestana
Karen Goldsmith-Pestana
YMYutaka Masuda
Yutaka Masuda
RFRichard A. Flavell
Richard A. Flavell
17 October 2006 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
ABAbdallah Badou
Abdallah Badou
MJMithilesh Kumar Jha
Mithilesh Kumar Jha
DMDidi Matza
Didi Matza
WMWajahat Z. Mehal
Wajahat Z. Mehal
MFMarc Freichel
Marc Freichel
RFRichard A. Flavell
Richard A. Flavell
Calcium ion is a universal signaling intermediate, which is known to control various biological processes. In excitable cells, voltage-gated calcium channels (Cav) are the major route of calcium entry and regulate multiple functions such as contraction, neurotransmitter release, and gene transcription. Here we show that T lymphocytes, which are nonexcitable cells, express both regulatory β and pore-forming Cav1 α1 subunits of Cav channels, and we provide genetic evidence for a critical role of the Cav β3 and Cav β4 regulatory subunits in T lymphocyte function. Cav β-deficient T lymphocytes fail to acquire normal functions, and they display impairment in the T cell receptor-mediated calcium response, nuclear factor of activated T cells activation, and cytokine production. In addition, unlike in excitable cells, our data suggest a minimal physiological role for depolarization in Cav channel opening in T cells. T cell receptor stimulation induces only a small depolarization of T cells, and artificial depolarization of T cells using KCl does not lead to calcium entry. These observations suggest that the Cav channels expressed by T cells have adopted novel regulation/gating mechanisms.