#ECTRIMS2019 – Is Rituximab a Reasonable Option for MS Patients?

#ECTRIMS2019 – Is Rituximab a Reasonable Option for MS Patients?

Publication date: Oct 04, 2019

*** More than two years after the approval of Ocrevus (ocrelizumab), B-cell therapies continue to be seen as promising approaches for multiple sclerosis (MS). But it has been debated if rituximab – a B-cell therapy used off-label in MS and also marketed by Genentech – could provide similar or even superior benefits compared with Ocrevus, and at a lower cost. This question was the focus of a hot topic discussion at the 35th Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), held Sept. 11-13 in Stockholm, where a group of researchers and neurologists voiced their opinions about whether or not rituximab is a reasonable alternative to Ocrevus for people with relapsing MS. Immune cells homing to the brain and spinal cord (the central nervous system, or CNS) to trigger local inflammation, demyelination (loss of myelin, the protective coat of neurons), and nerve cell death are central for MS. And B-cells, a type of white blood cells, have been identified as relevant players in this process. For this reason, immunosuppressive treatments that target B-cells have emerged as important therapeutic strategies for MS. Efforts have been focused on so-called anti-CD20 therapies – antibodies that pinpoint a specific protein on the surface of B-cells called CD20, targeting them for destruction and resulting in B-cell depletion. B-cell therapies make sense At ECTRIMS, the discussion started with neuroimmunologist David Baker, PhD, a professor at the Barts and The London School of Medicine and Dentistry in the U. K., speaking about the rationale for B-cell therapy in MS. -For many years, we’ve been told that MS is mediated by CD4+ Th17 T-cells,” Baker said, referring to a class of immune cells called T-cells, which are known to promote inflammation and play a role in the development of autoimmune diseases. Baker believes that B-cells, specifically memory B-cells, play a central role in MS. In his opinion, lower amounts of these cells in the CNS explain the response MS patients have to B-cell therapies, and possibly the origin and progression of the disease. Baker believes that MS therapies are only effective if they limit the ability of memory B-cells to enter the CNS. Additionally, Epstein-Barr virus (EBV), a proposed risk factor for MS, -affects essentially everybody with multiple sclerosis,” and EBV proteins can -activate many of the autoimmune risk genes, and induce memory B-cells. ” Baker believes that -B-cells are instrumental in targeting what drives the active lesions, which occur in relapsing and progressive MS. ” B-cells drive MS progression by producing cytokines [small protein messengers of the immune system], and may also -produce antibodies which .. . keep the microglia [white blood cells residing in the CNS] in an activated state. “

Concepts Keywords
35th Congress Cell therapy
Antibodies Antibodies
Antibody Sjögren syndrome
Autoimmune Genentech
Autoimmune Diseases Rituximab
B Cell CD20
B Cells Multiple sclerosis
Biogen Ocrelizumab
Blood Immunology
Blood Cancers RTT
Brain Monoclonal antibodies
CD20 Health
CD4 Medicine
Central Nervous System Medical specialties
Cerebrospinal Fluid Cell therapy
Clinical Trials MS
Congress Intravenous infusion
Cytokines Infections
David Baker
Demyelination
Disability
Epstein Barr Virus
Europe
Genentech
Genetic Variant
Hot Topic
Immune Memory
Immune System
Immunosuppressive
Inflammation
Infusion
Interact
Interferon Beta 1a
Intravenous
Intravenous Infusion
London
Medicine
Microglia
Multiple Sclerosis
Myelin
Nerve
Neurons
PhD
Placebo
Plasma Cells
Production Memory
Progressive
Rebif
Relapse
Rheumatoid Arthritis
Risk Factor
Rituxan
Rituximab
Specific Surface
Spinal Cord
Stockholm
T Cell
T Cells
Th17
Vasculitis
White Blood Cells

Semantics

Type Source Name
gene UNIPROT LAT2
disease MESH demyelination
disease MESH risk factor
drug DRUGBANK Nonoxynol-9
gene UNIPROT CSF2
drug DRUGBANK Tabalumab
drug DRUGBANK Atacicept
disease MESH infections
disease MESH autoimmune diseases
disease MESH development
gene UNIPROT PDC
pathway BSID Immune System
disease DOID vasculitis
disease MESH vasculitis
disease MESH vasculitis
pathway BSID Rheumatoid arthritis
disease DOID rheumatoid arthritis
disease MESH rheumatoid arthritis
disease MESH cancers
drug DRUGBANK Interferon beta-1a
disease MESH relapses
disease MESH inflammation
gene UNIPROT ARID1A
gene UNIPROT ADHFE1
drug DRUGBANK Ocrelizumab
disease MESH Multiple Sclerosis
disease DOID Multiple Sclerosis
gene UNIPROT SLC35G1
drug DRUGBANK Rituximab
gene UNIPROT DESI1
disease DOID PPMS
gene UNIPROT MS4A1

Similar

Original Article

Leave a Comment

Your email address will not be published. Required fields are marked *