Ramzi Khattar

ORCID: 0000-0001-6389-1072
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About
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Research Areas
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Hepatitis C virus research
  • T-cell and Retrovirus Studies
  • Cytomegalovirus and herpesvirus research
  • Hepatitis B Virus Studies
  • Diabetes and associated disorders
  • Viral Infections and Immunology Research
  • Liver Disease Diagnosis and Treatment
  • Immunotherapy and Immune Responses
  • interferon and immune responses
  • Immune cells in cancer
  • Renal Transplantation Outcomes and Treatments
  • Chemokine receptors and signaling
  • Reproductive System and Pregnancy
  • RNA regulation and disease
  • Monoclonal and Polyclonal Antibodies Research
  • HIV Research and Treatment
  • Animal Virus Infections Studies
  • Immunodeficiency and Autoimmune Disorders
  • Phagocytosis and Immune Regulation
  • Virology and Viral Diseases
  • Virus-based gene therapy research
  • Atherosclerosis and Cardiovascular Diseases
  • Neuroinflammation and Neurodegeneration Mechanisms

Toronto General Hospital
2015-2018

University Health Network
2010-2016

University of Toronto
2010-2016

Ubiquitination is a critical regulator of the host immune response to viral infection, and many viruses, including coronaviruses, encode proteins that target ubiquitination system. To explore link between coronavirus infection ubiquitin system, we asked whether protein degradation by 26S proteasome plays role in severe infections using murine model SARS-like pneumonitis induced hepatitis virus strain 1 (MHV-1). In vitro, pretreatment peritoneal macrophages with inhibitors (pyrrolidine...

10.1128/jvi.01219-10 article EN Journal of Virology 2010-09-23

Inflammation may be maladaptive to the control of viral infection when it impairs interferon (IFN) responses, enhancing replication and spread. Dysregulated immunity as a result inappropriate innate inflammatory responses is hallmark chronic infections such as, hepatitis B virus C (HCV). Previous studies from our laboratory have shown that expression an IFN-stimulated gene (ISG), ubiquitin-like protease (USP)18 upregulated in HCV infection, leading impaired hepatocyte IFN-α. We examined...

10.1128/jvi.02557-15 article EN cc-by Journal of Virology 2016-03-24

Summary Therapies that promote tolerance in solid organ transplantation will improve patient outcomes by eliminating the need for long‐term immunosuppression. To investigate mechanisms of rapamycin‐induced tolerance, C3H/HeJ mice were heterotopically transplanted with MHC‐mismatched hearts from BALB/ cJ and monitored rejection after a short course rapamycin treatment. Mice had received developed indefinite graft survival, whereas untreated all rejected their grafts within 9 days. In vitro ,...

10.1111/imm.12354 article EN Immunology 2014-07-03

Mounting effective innate and adaptive immune responses are critical for viral clearance the generation of long lasting immunity. It is known that production inhibitory factors may result in inability host to clear viruses, resulting chronic persistence. Fibrinogen-like protein 2 (FGL2) has been identified as a novel effector molecule CD4+CD25+ Foxp3+ regulatory T (Treg) cells inhibits activity by binding FCγRIIB expressed primarily on antigen presenting (APC). In this study, we show...

10.1371/journal.pone.0072309 article EN cc-by PLoS ONE 2013-10-11

CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) are critical to the maintenance of immune tolerance. Treg known utilize a number molecular pathways control responses and maintain homeostasis. Fibrinogen-like protein 2 (FGL2) has been identified by investigators as an important immunosuppressive effector Treg, which exerts its immunoregulatory activity binding inhibitory FcγRIIB receptors expressed on antigen-presenting including dendritic cells, endothelial B cells. More recently, it...

10.5041/rmmj.10209 article EN cc-by Rambam Maimonides Medical Journal 2015-07-30

Fibrinogen-like protein 2 (FGL2) is an immunomodulatory that expressed by regulatory T cells (Tregs). The objective of this study was to determine if recombinant FGL2 (rFGL2) treatment or constitutive overexpression could promote transplant tolerance in mice. Although rFGL2 prevented rejection fully mismatched cardiac allografts, all grafts were rejected after stopping treatment. Next, we generated transgenic mice (fgl2(Tg) ) ubiquitously overexpressed FGL2. These developed normally and had...

10.1111/ajt.13696 article EN cc-by-nc-nd American Journal of Transplantation 2015-12-31

Persistent viruses evade immune detection by interfering with virus-specific innate and adaptive antiviral responses. Fibrinogen-like protein-2 (FGL2) is a potent effector molecule of CD4+ CD25+ FoxP3+ regulatory T cells exerts its immunosuppressive activity following ligation to cognate receptor, FcγRIIB/RIII. The role FGL2 in the pathogenesis chronic viral infection caused lymphocytic choriomeningitis virus clone-13 (LCMV cl-13) was assessed this study. Chronically infected fgl2+/+ mice...

10.1111/imm.12897 article EN Immunology 2018-01-17

High quality acute flaccid paralysis (AFP) surveillance is required to maintain polio-free status of a country. Papua New Guinea (PNG) considered as one the highest risk countries for polio re-importation and circulation in Western Pacific Region (WPRO) World Health Organization due poor healthcare infrastructure inadequate performance AFP surveillance. The Government PNG, collaboration with WHO, piloted introduction short-message-service (SMS) sensitize pediatricians provincial disease...

10.1186/s12889-016-3062-5 article EN cc-by BMC Public Health 2016-05-16

Urbanellis, P.1; Wang, J.2; Shalev, I.2; He, W.2; Adeyi, O. A.3; Phillips, M. J.3; Bartczak, A.2; Khattar, R.2; Grant, D. R.3; Levy, G. A.3 Author Information

10.1097/00007890-201007272-00098 article EN Transplantation 2010-07-01

Bartczak, A.; He, W.; Shalev, I.; Mendicino, M.; Zhang, J.; Ma, X.; Urbanellis, P.; Khattar, R.; Kaplovitch, E.; Phillips, M. Adeyi, O. Grant, D. Levy, G. A. Author Information

10.1097/00007890-201007272-00368 article EN Transplantation 2010-07-01

Abstract FGL2 is an effector molecule of CD4+CD25+FoxP3+ T regulatory cells (Treg) which exerts its effect through binding to FcγRIIb and FcγRIII on APC. Mice deficient in fgl2 show impaired Treg activity associated with increased immune reactivity development autoimmune glomerulonephritis. In a fully mismatched model heart allotransplantation where recipients were treated recombinant FGL2, graft survival was extended significantly but grafts rejected following cessation treatment. To...

10.4049/jimmunol.184.supp.145.37 article EN The Journal of Immunology 2010-04-01
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