Raymond A. Sobel

ORCID: 0000-0002-0477-9002
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About
Contact & Profiles
Research Areas
  • T-cell and B-cell Immunology
  • Immune Cell Function and Interaction
  • Immunotherapy and Immune Responses
  • Monoclonal and Polyclonal Antibodies Research
  • Multiple Sclerosis Research Studies
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Immune Response and Inflammation
  • Galectins and Cancer Biology
  • Cytokine Signaling Pathways and Interactions
  • Antifungal resistance and susceptibility
  • Fungal Infections and Studies
  • Glioma Diagnosis and Treatment
  • Cell Adhesion Molecules Research
  • Glycosylation and Glycoproteins Research
  • Systemic Lupus Erythematosus Research
  • RNA Interference and Gene Delivery
  • interferon and immune responses
  • Peripheral Neuropathies and Disorders
  • Neurofibromatosis and Schwannoma Cases
  • Peptidase Inhibition and Analysis
  • Diabetes and associated disorders
  • RNA Research and Splicing
  • Peroxisome Proliferator-Activated Receptors
  • CAR-T cell therapy research
  • Viral Infections and Immunology Research

Stanford University
2016-2025

VA Palo Alto Health Care System
2014-2025

University of California, San Francisco
2014-2023

Washington University in St. Louis
2023

Chan Zuckerberg Initiative (United States)
2023

Cancer Institute (WIA)
2023

United States Department of Veterans Affairs
1981-2017

Stratford University
2017

Australian Regenerative Medicine Institute
2014-2016

Monash University
2014-2016

Multiple sclerosis (MS) is considered to be an autoimmune disease of the central nervous system (CNS) that in many patients first presents clinically as optic neuritis. The relationship neuritis MS not well understood. We have generated novel T cell receptor (TCR) transgenic mice specific for myelin oligodendrocyte glycoprotein (MOG). MOG-specific cells are deleted nor tolerized and functionally competent. A large proportion (>30%) TCR spontaneously develop isolated without any...

10.1084/jem.20021603 article EN The Journal of Experimental Medicine 2003-05-05

Experimental autoimmune encephalomyelitis (EAE) is a model of human multiple sclerosis induced by autoreactive Th cells that mediate tissue inflammation and demyelination in the CNS. Initially, IFN-gamma-producing Th1 and, more recently, IL-17-producing Th17 with specificity for myelin Ags have been implicated EAE induction, but whether are encephalitogenic has controversial. Moreover, new effector T cell subset, Th9 cells, identified; however, ability this subset to induce not investigated....

10.4049/jimmunol.0901906 article EN The Journal of Immunology 2009-11-05

Multiple sclerosis is a demyelinating disease, characterized by inflammation in the brain and spinal cord, possibly due to autoimmunity. Large-scale sequencing of cDNA libraries, derived from plaques dissected brains patients with multiple (MS), indicated an abundance transcripts for osteopontin (OPN). Microarray analysis cords rats paralyzed experimental autoimmune encephalomyelitis (EAE), model MS, also revealed increased OPN transcripts. Osteopontin-deficient mice were resistant...

10.1100/tsw.2002.326 article EN 2002-04-12

Both positive and negative regulatory roles have been suggested for the B7 family member PD-L1(B7-H1). PD-L1 is expressed on antigen-presenting cells (APCs), activated T cells, a variety of tissues, but functional significance each cell type not yet clear. To dissect functions in vivo , we generated PD-L1-deficient (PD-L1 –/– ) mice. CD4 + CD8 responses were markedly enhanced mice compared with wild-type vitro . dendritic stimulated greater than produced more cytokines demonstrating an...

10.1073/pnas.0307252101 article EN Proceedings of the National Academy of Sciences 2004-07-12

Abstract Experimental autoimmune encephalomyelitis (EAE) and other organ-specific diseases are induced by autoantigen-specific Th1 cells. In contrast, transfer of autoantigen-reactive Th2 cells that produce IL-4 IL-10 can prevent and/or reverse EAE. The relative roles these two cytokines in the regulation EAE has not been evaluated. Utilizing knockout mice deficient for transgenic overexpressing cytokines, we demonstrate IL-10-deficient (IL-10−/−) more susceptible develop a severe when...

10.4049/jimmunol.161.7.3299 article EN The Journal of Immunology 1998-10-01

The transcription factors signal transducer and activator of (STAT)1 T-bet control the differentiation interferon (IFN)-γ–producing T helper type (Th)1 cells. Here we compare role STAT1 in initiation regulation experimental autoimmune encephalomyelitis (EAE), a disease initiated by Th1 T-bet–deficient mice immunized with myelin oligodendrocyte glycoprotein (MOG) were resistant to development EAE. This protection was also observed when T-bet−/− crossed MOG-specific 2D2 cell receptor...

10.1084/jem.20031819 article EN The Journal of Experimental Medicine 2004-07-05

Local catabolism of the amino acid tryptophan (Trp) by indoleamine 2,3-dioxygenase (IDO) is considered an important mechanism regulating T cell immunity. We show that IDO transcription was increased when myelin-specific cells were stimulated with tolerogenic altered self-peptides. Catabolites Trp suppressed proliferation and inhibited production proinflammatory helper-1 (T(H)1) cytokines. N-(3,4,-Dimethoxycinnamoyl) anthranilic (3,4-DAA), orally active synthetic derivative metabolite acid,...

10.1126/science.1117634 article EN Science 2005-11-03

Abstract Human T‐cell lymphotropic virus type III (HTLV‐III) has been isolated from neural tissues and cerebrospinal fluid (CSF) of patients with neurological syndromes associated the acquired immune deficiency syndrome (AIDS) may be directly involved in pathogenesis syndromes. To detect HTLV‐III antigen AIDS, immunoperoxidase studies using a goat anti‐HTLV‐III serum were performed on frozen tissue sections brain, spinal cord, nerve 13 AIDS or HTLV‐III–related was cultured CSF 11 these...

10.1002/ana.410200304 article EN Annals of Neurology 1986-09-01

Whether B cells serve as antigen-presenting (APCs) for activation of pathogenic T in the multiple sclerosis model experimental autoimmune encephalomyelitis (EAE) is unclear. To evaluate their role APCs, we engineered mice selectively deficient MHC II on (B–MHC II−/−), and to distinguish this function from antibody production, created transgenic (Tg) that express myelin oligodendrocyte glycoprotein (MOG)–specific cell receptor (BCR; IgHMOG-mem) but cannot secrete antibodies. B–MHC II−/− were...

10.1084/jem.20130699 article EN cc-by-nc-sa The Journal of Experimental Medicine 2013-12-09

Abstract PLP is the major protein constituent of central nervous system myelin. We have previously shown that SJL/J (H-2s) mice develop an acute form EAE after immunization with PLP. The purpose present study was to identify encephalitogenic determinant for SJL mice. immunized a synthetic peptide identical residues 130-147 QAHSLERVCHCLGKWLGH murine PLP, sequence having amphipathic alpha-helical conformation. Although it did not induce disease, overlapping containing 139-154 HCLGKWLGHPDKFVGI...

10.4049/jimmunol.142.5.1523 article EN The Journal of Immunology 1989-03-01

The factors contributing to chronic relapsing inflammatory disease processes of the central nervous system (CNS) and demyelination are poorly understood. In addition cellular immune reactions, humoral such as antibodies might quantitatively or qualitatively influence process. We therefore investigated effects administration a monoclonal antibody specific for CNS autoantigen on both acute experimental autoimmune encephalomyelitis (EAE) in mice rats. This antibody, 8-18C5,...

10.4049/jimmunol.139.12.4016 article EN The Journal of Immunology 1987-12-15
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