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Cited by 135Multiple Sclerosis Research StudiesT-cell and B-cell ImmunologyPsoriasis: Treatment and Pathogenesis

The DOI matches its Crossref record; 126 of the 126 references it cites were found in a registry or an index.

Glatiramer acetate: mechanisms of action in multiple sclerosis.

Ziemssen, Tjalf, Schrempf, Wiebke·2007·International review of neurobiology
DOI 10.1016/s0074-7742(07)79024-4
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Abstract

Glatiramer acetate (GA), formerly known as copolymer 1, is a mixture of synthetic polypeptides composed of four amino acids resembling the myelin basic protein (MSP). GA has been shown to be highly effective in preventing and suppressing experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). Therefore, it was tested in several clinical studies and so approved for the immunomodulatory treatment of relapsing-type MS. In contrast to other immunomodulatory MS therapies, GA has a distinct mechanism of action: GA demonstrates an initial strong promiscuous binding to major histocompatibility complex molecules and consequent competition with various (myelin) antigens for their presentation to T cells. In addition, antigen-based therapy generating a GA-specific immune response seems to be the prerequisite for GA therapy. GA treatment induces an in vivo change of the frequency, cytokine secretion pattern and the effector function of GA-specific CD4+ and CD8+ T cells, probably by affecting the properties of antigen-presenting cells such as monocytes and dendritic cells. As demonstrated extensively in animal experiments, GA-specific, mostly, T helper 2 cells migrate to the brain and lead to in situ bystander suppression of the inflammatory process in the brain. Furthermore, GA-specific cells in the brain express neurotrophic factors like the brain-derived neurotrophic factor (BDNF) in addition to anti-inflammatory T helper 2-like cytokines. This might help tip the balance in favor of more beneficial influences because there is a complex interplay between detrimental and beneficial factors and mediators in the inflammatory milieu of MS lesions.

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Crossref · 10.1016/s0074-7742(07)79024-4

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Research works printed but not linked: 1

  1. Serpe, 1999, Exacerbation of facial motor‐neuron loss after facial nerve transection in severe combined immunodeficient (SCID) mice, J. Neurosci., RC7, 1

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Metadata

Authors
Ziemssen, T., & Schrempf, W.
Affiliations
Technische Universität Dresden (DE)
ORCID
Ziemssen, Tjalf
Venue
International review of neurobiology
Publisher
Elsevier
Published
2007
Volume
79
Pages
537-570
ISSN
0074-7742 (ISSN-L)
DOI
10.1016/s0074-7742(07)79024-4
OpenAlex
W1906718334
Cited by
135
References
126
Citations by year
2025: 2 · 2024: 3 · 2023: 2 · 2022: 2 · 2021: 8 · 2020: 12 · 2019: 7 · 2018: 7 · 2017: 3 · 2016: 14 · 2015: 9 · 2014: 8 · 2013: 5 · 2012: 7
FWCI
42.44
Type
book chapter
Language
en
Open access
closed
Locations
  • International review of neurobiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Keywords
glatiramer acetate, multiple sclerosis, mechanism of action, myelin basic protein, experimental autoimmune encephalomyelitis, MHC binding, antigen presentation, T cell regulation, dendritic cells, monocytes, antigen-presenting cells, Th2 cells, bystander suppression, brain-derived neurotrophic factor, neurotrophic factors, immunomodulatory therapy, cytokine production
MeSH terms
Glatiramer Acetate, Animals, Disease Models, Animal, Humans, Immunosuppressive Agents, Lymphocyte Activation, Lymphocytes, Multiple Sclerosis, Peptides, Brain-Derived Neurotrophic Factor

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