Samia J. Khoury

ORCID: 0000-0003-3198-6063
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About
Contact & Profiles
Research Areas
  • Multiple Sclerosis Research Studies
  • T-cell and B-cell Immunology
  • Immunotherapy and Immune Responses
  • Immune Cell Function and Interaction
  • Peripheral Neuropathies and Disorders
  • Systemic Lupus Erythematosus Research
  • Polyomavirus and related diseases
  • Immune Response and Inflammation
  • Cytokine Signaling Pathways and Interactions
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neurogenesis and neuroplasticity mechanisms
  • Rheumatoid Arthritis Research and Therapies
  • Monoclonal and Polyclonal Antibodies Research
  • Systemic Sclerosis and Related Diseases
  • Diabetes and associated disorders
  • MicroRNA in disease regulation
  • Autoimmune and Inflammatory Disorders Research
  • Reproductive System and Pregnancy
  • NF-κB Signaling Pathways
  • Viral Infections and Immunology Research
  • RNA regulation and disease
  • Acute Lymphoblastic Leukemia research
  • Biotin and Related Studies
  • Health Systems, Economic Evaluations, Quality of Life
  • Fibromyalgia and Chronic Fatigue Syndrome Research

American University of Beirut Medical Center
2016-2025

American University of Beirut
2016-2025

Tel Aviv University
2025

Biogen (Switzerland)
2024

Karolinska Institutet
2018-2024

Walton Centre
2024

Monash University
2024

University of Liverpool
2024

University of Pennsylvania
2023-2024

Johns Hopkins Medicine
2023-2024

Migration toward pathology is the first critical step in stem cell engagement during regeneration. Neural cells (NSCs) migrate through parenchyma along nonstereotypical routes a precise directed manner across great distances to injury sites CNS, where they might engage niches harboring local transiently expressed reparative signals. The molecular mechanisms for NSC mobilization have not been identified. Because NSCs seem home similarly pathologic derived from disparate etiologies, we...

10.1073/pnas.0408258102 article EN Proceedings of the National Academy of Sciences 2004-12-17

Programmed death-1 (PD-1) receptor, an inhibitory costimulatory molecule found on activated T cells, has been demonstrated to play a role in the regulation of immune responses and peripheral tolerance. We investigated this pathway development autoimmune diabetes. PD-1 or PD-L1 but not PD-L2 blockade rapidly precipitated diabetes prediabetic female nonobese diabetic (NOD) mice regardless age (from 1 10-wk-old), although it was most pronounced older mice. By contrast, cytotoxic...

10.1084/jem.20022125 article EN The Journal of Experimental Medicine 2003-07-07

Experimental autoimmune encephalomyelitis (EAE) in the Lewis rat is a self-limited inflammatory process localized to central nervous system that induced by injection of myelin basic protein (MBP) adjuvant. Oral administration MBP suppresses EAE, and this suppression mediated CD8+ T cells adoptively transfer protection suppress both vitro vivo release transforming growth factor (TGF) beta after antigen-specific triggering. Furthermore, oral tolerance enhanced concomitant lipopolysaccharide...

10.1084/jem.176.5.1355 article EN The Journal of Experimental Medicine 1992-11-01

Multiple sclerosis (MS) is thought to be an autoimmune disease mediated by T lymphocytes that recognize myelin components of the central nervous system. In a 1-year double-blind study, 30 individuals with relapsing-remitting MS received daily capsules bovine or control protein determine effect oral tolerization antigens on disease. Six 15 in myelin-treated group had at least one major exacerbation; 12 attack group. cells reactive basic were reduced No toxicity side effects noted. Although...

10.1126/science.7680493 article EN Science 1993-02-26

Abstract Little is known about how neurons in the different layers of mammalian cerebral cortex are specified at molecular level. Expression two homologues Drosophila homeobox Cut gene, Cux‐1 and Cux‐2 , strikingly specific to pyramidal upper (II–IV) murine cortex, suggesting that they may define identity these neurons. An antibody against labels nucleus most postmitotic layer but does not label parvoalbumin‐positive cortical interneurons derive from medial ganglionic eminence. represent...

10.1002/cne.20322 article EN The Journal of Comparative Neurology 2004-09-27

Oral administration of antigen is a long recognized method inducing systemic immune tolerance. In animals with experimental autoimmune disease, major mechanism oral tolerance triggered by involves the induction regulatory T cells that mediate active suppression secreting cytokine TGF-beta 1. Multiple sclerosis (MS) presumed cell-mediated Th1 type disease. Here, we investigated whether in MS patients myelin treatment, containing both basic protein (MBP) and proteolipid (PLP), induced specific...

10.1172/jci118779 article EN Journal of Clinical Investigation 1996-07-01

Experimental autoimmune encephalomyelitis (EAE) is mediated by autoantigen-specific T cells dependent on critical costimulatory signals for their full activation and regulation. We report that the programmed death-1 (PD-1) pathway plays a role in regulating peripheral tolerance murine EAE appears to be major contributor resistance of disease induction CD28-deficient mice. After immunization with myelin oligodendrocyte glycoprotein (MOG) there was progressive increase expression PD-1 its...

10.1084/jem.20022119 article EN The Journal of Experimental Medicine 2003-07-07

The development of T helper (T(H))17 and regulatory (T(reg)) cells is reciprocally regulated by cytokines. Transforming growth factor (TGF)-beta alone induces FoxP3(+) T(reg) cells, but together with IL-6 or IL-21 T(H)17 cells. Here we demonstrate that IL-9 a key molecule affects differentiation function. predominantly produced synergizes TGF-beta1 to differentiate naïve CD4(+) into while secretion IL-23. Interestingly, enhances the suppressive functions in vitro, absence signaling weakens...

10.1073/pnas.0812530106 article EN Proceedings of the National Academy of Sciences 2009-05-12

Fetal survival during gestation implies that tolerance mechanisms suppress the maternal immune response to paternally inherited alloantigens. Here we show inhibitory T cell costimulatory molecule, programmed death ligand 1 (PDL1), has an important role in conferring fetomaternal allogeneic pregnancy model. Blockade of PDL1 signaling murine resulted increased rejection rates concepti but not syngeneic concepti. was cell- B cell-dependent because PDL1-specific antibody treatment caused fetal...

10.1084/jem.20050019 article EN The Journal of Experimental Medicine 2005-07-18

Abstract Innate immune cells may regulate adaptive immunity by balancing different lineages of T and providing negative costimulation. In addition, CD11b+Gr-1+ myeloid-derived suppressor have been described in tumor, parasite infection, severe trauma models. this study, we observe that splenic CD11b+ markedly increase after experimental autoimmune encephalomyelitis (EAE) immunization, they suppress cell proliferation vitro. Although >80% express varying levels Gr-1, only a small...

10.4049/jimmunol.179.8.5228 article EN The Journal of Immunology 2007-10-15

MicroRNAs (miRNAs) are single-stranded, small noncoding RNAs that regulate gene expression. Because they stable in serum, being developed as biomarkers for cancer and other diseases. In multiple sclerosis (MS), miRNAs have been studied cell populations but not the circulation. MS, a major challenge is to develop immune monitor disease. We asked whether circulating could be identified MS linked disease stage and/or disability.A total of 368 were measured ethylenediaminetetraacetic acid plasma...

10.1002/ana.23880 article EN Annals of Neurology 2013-03-14

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system postulated to be cell-mediated autoimmune in which interferon γ (IFN-γ) plays an important role. There increased IFN-γ secretion MS, and administration induces exacerbations disease. We found that interleukin 12 (IL-12) was responsible for raised MS as anti-IL-12 antibodies reversed anti-CD3-induced patients normal levels. Furthermore, we marked increase T cell receptor-mediated IL-12 progressive vs....

10.1073/pnas.94.2.599 article EN Proceedings of the National Academy of Sciences 1997-01-21

The onset of neurological signs in experimental autoimmune encephalomyelitis is tightly associated with infiltration and reactivation T cells the central nervous system. anatomic localization initial cell-antigen-presenting cell (APC) interactions leading to system is, however, still unclear. We hypothesized that activated CD4(+) gain direct access subarachnoid space become reactivated on encounter cognate antigen this compartment.

10.1002/ana.21379 article EN Annals of Neurology 2008-05-21

CD8+ T cell depletion renders CD28-deficient mice susceptible to experimental autoimmune encephalomyelitis (EAE). In addition, CD8–/–CD28–/– double-knockout are EAE. These findings suggest a role for cells in the resistance of disease. Adoptive transfer CD8+CD28– into CD8–/– results significant suppression disease, while CD8+CD28+ demonstrate no similar effect on clinical course EAE same recipients. vitro, but not suppress IFN-γ production myelin oligodendrocyte glycoprotein–specific CD4+...

10.1172/jci17935 article EN Journal of Clinical Investigation 2003-10-01

Multiple sclerosis (MS) is a chronic relapsing disease of the central nervous system (CNS) in which immune processes are believed to play major role. To date, there no reliable method by characterize and their changes associated with different forms MS progression. We performed antigen microarray analysis patterns antibody reactivity serum against panel CNS protein lipid autoantigens heat shock proteins. Informatic consisted training set that was validated on blinded test set. The results...

10.1073/pnas.0806310105 article EN Proceedings of the National Academy of Sciences 2008-11-22

<h3>Background</h3> Although cigarette smokers are at increased risk of developing multiple sclerosis (MS), the effect smoking on progression MS remains uncertain. <h3>Objective</h3> To establish relationship between and using clinical magnetic resonance imaging outcomes <h3>Design</h3> Cross-sectional survey longitudinal follow-up for a mean 3.29 years, ending January 15, 2008. <h3>Setting</h3> Partners Center (Boston, Massachusetts), referral center patients with MS. <h3>Patients</h3>...

10.1001/archneurol.2009.122 article EN Archives of Neurology 2009-07-01
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