Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Secondary progressive in contrast to relapsing-remitting multiple sclerosis patients show a normal CD4+CD25+ regulatory T-cell function and FOXP3 expression.

Journal of neuroscience research - 1 Jun 2006

Venken Koen, Hellings Niels, Hensen Karen, Rummens Jean-Luc, Medaer Robert, D'hooghe Marie B, Dubois Bénédicte, Raus Jef, Stinissen Piet

Abstract excerpt

Accumulating evidence indicates an immunosuppressive role for CD4(+)CD25(+) regulatory T cells (Tregs) in autoimmune diseases. Although an impaired Treg function in patients with relapsing-remitting multiple sclerosis (RR-MS) has been reported recently, no information is available so far about Treg function in the progressive stage of the disease. In the present study, the phenotypic and functional...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to CD4-Positive T-Lymphocytes
Share to Forkhead Transcription Factors

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Immune Tolerance

Share to Interferon-gamma

Share to Multiple Sclerosis, Chronic Progressive

Share to Multiple Sclerosis, Relapsing-Remitting

Share to Receptors, Interleukin-2

Share to T-Lymphocytes, Regulatory

Source

Identifiers

PMID: 16583400
DOI: 10.1002/jnr.20852

Genes

FOXP3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Secondary progressive in contrast to relapsing-remitting multiple sclerosis patients show a normal CD4+CD25+ regulatory T-cell function and FOXP3 expression.PMID 16583400Read ↗

Patients With Severe Multiple Sclerosis Exhibit Functionally Altered CD8 + Regulatory T CellsSemantic proximity Read ↗

Ex vivo expanded regulatory T cells CD4+CD25+FoxP3+CD127Low develop strong immunosuppressive activity in patients with remitting-relapsing multiple sclerosis.Semantic proximity Read ↗

Unaltered regulatory B-cell frequency and function in patients with multiple sclerosis.Semantic proximity Read ↗

Encephalitogenic and Regulatory CD8 T Cells in Multiple Sclerosis and Its Animal ModelsSemantic proximity Read ↗

Targeting Impaired Type I Interferon–IL-27 Signaling Rescues T Regulatory Cell Suppressive Function in Relapsing-Remitting Multiple SclerosisSemantic proximity Read ↗

Regulatory T cells promote myelin regeneration in the central nervous systemSemantic proximity Read ↗

CD4(+)CD25(+)CD127(-) and CD4(+)CD25(+)Foxp3(+) Regulatory T Cell Subsets in Mediating Autoimmune Reactivity in Systemic Lupus Erythematosus Patients.Semantic proximity Read ↗

CD4(+)CD25(+) regulatory T cells in rheumatoid arthritis: differences in the presence, phenotype, and function between peripheral blood and synovial fluid.Semantic proximity Read ↗

MiR-9-5p and miR-106a-5p dysregulated in CD4+ T-cells of multiple sclerosis patients and targeted essential factors of T helper17/regulatory T-cells differentiation.Semantic proximity Read ↗

The interleukin-7 receptor α chain contributes to altered homeostasis of regulatory T cells in multiple sclerosis.Semantic proximity Read ↗

Comprehensive analysis of miRNA expression in T-cell subsets of rheumatoid arthritis patients reveals defined signatures of naive and memory TregsSemantic proximity Read ↗

miR-141 and miR-200a, Revelation of New Possible Players in Modulation of Th17/Treg Differentiation and Pathogenesis of Multiple SclerosisSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.