Clinical trial NCT00819195: Anti-Inflammatory Type II Monocyte Induction by Glatiramer Acetate (Copaxone) Treatment of Multiple Sclerosis
Official title: Anti-Inflammatory Type II Monocyte Induction by Glatiramer Acetate (Copaxone) Treatment of Multiple Sclerosis
Study type: OBSERVATIONAL
Overall status: COMPLETED
Conditions: Multiple Sclerosis
Keywords: relapsing-remitting
multiple sclerosis
Copaxone
glatiramer acetate
MS
Lead sponsor: University of California, San Francisco
Sponsor class: OTHER
Collaborators: name: National Multiple Sclerosis Society
name: Teva Neuroscience, Inc.
First posted: 2009-01-08
Enrollment: 17
Sex: ALL
Minimum age (years): 18
Maximum age (years): 55
Standard ages: ADULT
Accepts healthy volunteers: yes
Observational model: COHORT
Time perspective: PROSPECTIVE
Sampling method: NON_PROBABILITY_SAMPLE
Study population: Relapsing-remitting multiple sclerosis patients at the UCSF Multiple Sclerosis Center.

Brief summary: The purpose of this study is to determine whether glatiramer acetate (Copaxone) will induce anti-inflammatory type II monocyte development during treatment of MS, and if these antigen presenting cells (APC) will promote Th2 and Treg differentiation of naïve T cells.


Eligibility criteria: Inclusion Criteria:

* Relapsing-remitting (RR) MS patients (McDonald criteria)
* Ages 18-55
* Males and females
* EDSS score ≤5
* No prior treatment with Copaxone
* Prior treatment with corticosteroids or interferon-beta (-1a or -1b) is acceptable, provided there is a washout period of at least one month

Exclusion Criteria:

* Treatment with Tysabri, Novantrone or cyclophosphamide
* Treatment with other immunomodulatory therapies (e.g. imuran, mycophenolate or methotrexate)
* Primary-progressive (PP) and secondary-progressive (SP) multiple sclerosis
* Pregnancy

Primary outcomes:
measure: Production of inflammatory cytokines by monocytes and naive T cells.
timeFrame: 0, 1, 2, 4, 6 months
Secondary outcomes:
Other outcomes:
Locations:
city: San Francisco
country: United States
facility: UCSF Multiple Sclerosis Center
state: California
Study officials:
affiliation: UCSF Department of Neurology
name: Scott S. Zamvil, M.D. Ph.D.
role: PRINCIPAL_INVESTIGATOR
References:
citation: Weber MS, Prod'homme T, Youssef S, Dunn SE, Rundle CD, Lee L, Patarroyo JC, Stuve O, Sobel RA, Steinman L, Zamvil SS. Type II monocytes modulate T cell-mediated central nervous system autoimmune disease. Nat Med. 2007 Aug;13(8):935-43. doi: 10.1038/nm1620. Epub 2007 Aug 5.
citation: Neuhaus O, Farina C, Wekerle H, Hohlfeld R. Mechanisms of action of glatiramer acetate in multiple sclerosis. Neurology. 2001 Mar 27;56(6):702-8. doi: 10.1212/wnl.56.6.702. No abstract available.
citation: Farina C, Weber MS, Meinl E, Wekerle H, Hohlfeld R. Glatiramer acetate in multiple sclerosis: update on potential mechanisms of action. Lancet Neurol. 2005 Sep;4(9):567-75. doi: 10.1016/S1474-4422(05)70167-8.
citation: Kim HJ, Ifergan I, Antel JP, Seguin R, Duddy M, Lapierre Y, Jalili F, Bar-Or A. Type 2 monocyte and microglia differentiation mediated by glatiramer acetate therapy in patients with multiple sclerosis. J Immunol. 2004 Jun 1;172(11):7144-53. doi: 10.4049/jimmunol.172.11.7144.
citation: Weber MS, Starck M, Wagenpfeil S, Meinl E, Hohlfeld R, Farina C. Multiple sclerosis: glatiramer acetate inhibits monocyte reactivity in vitro and in vivo. Brain. 2004 Jun;127(Pt 6):1370-8. doi: 10.1093/brain/awh163. Epub 2004 Apr 16.