Targeting a rogue T cell prevents and reverses multiple sclerosis in mice

Targeting a rogue T cell prevents and reverses multiple sclerosis in mice

Publication date: Oct 05, 2019

T helper cells bearing the CXCR6 surface marker drive multiple sclerosis by producing a host of proteins that damage nerve fibers, by attacking their protective myelin sheath.

It’s driven by “helper” T cells, white blood cells that mount an inflammatory attack on the brain and spinal cord, degrading the protective myelin sheath that covers nerve fibers.

Researchers at Boston Children’s Hospital have now pinpointed the specific helper T cells that cause MS, as well as a protein on their surface that marks them.

If human studies bear out the findings, targeting these rogue T cells could potentially ameliorate MS, says senior investigator Eileen Remold-O’Donnell, PhD, of the hospital’s Program in Cellular and Molecular Medicine.

These cells, they showed, are highly damaging to nerve fibers, producing one set of proteins that directly damage cells and others, including GM-CSF, that stimulate an inflammatory attack by other immune cells known as macrophages.

When they deleted the Sb1 gene in T cells in their mouse model, fewer immune cells survived to infiltrate the spinal cord.

T helper cells bearing the CXCR6 marker drive multiple sclerosis by producing proteins that damage nerve fibers by attacking their protective myelin sheath.

Credit: Lifei Hou/Boston Children’s Hospital Targeting CXCR6 in multiple sclerosis Remold-O’Donnell and Hou, first author on the paper, believe treatments to deplete CXCR6+ cells could mitigate MS and possibly other autoimmune disorders while largely leaving other T cell immune defenses intact.

Concepts Keywords
Antibodies Antibodies
Antibody Neuroinflammation
Arthritis CXCR6
Autoimmune Autoimmunity
Autoimmune Diseases Myelitis
Autoimmune Disorders CXC chemokine receptors
Bear Myelin
Blood Neurology
Boston Immunology
Brain Chemokine receptors
Childrens Hospital Medicine
Cytotoxic Medical specialties
Edelweiss Immunosuppression
Encephalomyelitis Autoimmune diseases
Equity Blood arthritis
Fair Dealing Relevant disease
Glucocorticoids Autoimmune disorders
Hospital
Immune Cells
Immunosuppression
Immunosuppressive Agents
Inflammation
Macrophages
Mice
Monoclonal Antibodies
Mount
Multiple Sclerosis
Myelin Sheath
Nerve
Patent
Pathogenic
PhD
PNAS
Postdoctoral Fellow
Protein
Spinal Cord
Synovial Fluid
TH17
TH17 Cells

Semantics

Type Source Name
gene UNIPROT CXCR6
disease MESH multiple sclerosis
disease DOID multiple sclerosis
gene UNIPROT PDC
disease MESH encephalomyelitis
disease DOID encephalomyelitis
disease MESH inflammation
disease MESH arthritis
disease DOID arthritis
gene UNIPROT SET
gene UNIPROT SERPINB1
gene UNIPROT SHKBP1
drug DRUGBANK Tropicamide
gene UNIPROT BAD
disease DOID autoimmune disease
disease MESH autoimmune disease
pathway BSID Release
gene UNIPROT CSF2
drug DRUGBANK Sargramostim
gene UNIPROT MAGEE1

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