CTLA4Ig treatment in patients with multiple sclerosis  

Oleh:

Viglietta, V. ; Bourcier, K. ; Buckle, G. J.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Neurology (Official Journal of The American Academy of Neurology) vol. 71 no. 12 (Sep. 2008), page 917-924.
Topik: INTERFERON; INTERLEUKIN; RHEUMATOID ARTHRITIS; URINARY TRACT INFECTION; WHITE BLOOD CELL

Ketersediaan

Perpustakaan FK Nomor Panggil: N11.K.2008.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Background: The modulation of costimulatory pathways represents an original therapeutic approach to regulate T cell–mediated autoimmune diseases by preventing or reducing autoantigen-driven T-cell activation in humans. Autoreactive CD4+ T cells play a critical role in initiating the immune response leading to the chronic inflammation and demyelination characteristic of multiple sclerosis (MS). Methods: We used IV infusions of CTLA4Ig to block the CD28/B7 T-cell costimulatory pathway in a phase 1 dose-escalation study in MS. Sixteen patients with relapsing–remitting MS received a single CTLA4Ig infusion and were monitored for up to 3 months after treatment. In an extension study, four additional subjects received four doses of CTLA4Ig. Results: CTLA4Ig was well tolerated in patients with MS, and most adverse events were rated as mild. Immunologic assessment of the patients showed a reduction in myelin basic protein (MBP) proliferation within 2 months of infusion and decreased interferon-{gamma} production by MBP-specific lines. Conclusions: Inhibiting costimulatory molecule interactions by using CTLA4Ig seems safe in multiple sclerosis (MS), and the immunologic effects suggest that it may be a promising approach to regulate the inflammatory process associated with MS.

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