Assessment of different treatment failure criteria in a cohort of relapsing-remitting multiple sclerosis patients treated with interferon β: Implications for clinical trials

2002 ◽  
Vol 52 (4) ◽  
pp. 400-406 ◽  
Author(s):  
Jordi Río ◽  
Carlos Nos ◽  
Mar Tintoré ◽  
Cecilia Borrás ◽  
Ingrid Galán ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Clinical Trials ◽  
Treatment Failure ◽  
Failure Criteria ◽  
Interferon Β ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Multiple Sclerosis Patients ◽  
Relapsing Remitting Multiple Sclerosis

Immunoglobulin-like transcript 3, an inhibitor of T cell activation, is reduced on blood monocytes during multiple sclerosis relapses and is induced by interferon β-1b

2009 ◽  
Vol 16 (1) ◽  
pp. 30-38 ◽  
Author(s):  
Mark A Jensen ◽  
Rachel N Yanowitch ◽  
Anthony T Reder ◽  
David M White ◽  
Barry GW Arnason
Keyword(s):  
Multiple Sclerosis ◽  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Mononuclear Cells ◽  
Interferon Β ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Multiple Sclerosis Patients ◽  
Relapsing Remitting Multiple Sclerosis

Immunoglobulin-like transcripts (ILTs) are immunoregulatory proteins that either activate or inhibit immune responses. ILT3 is inhibitory and is expressed preferentially by antigen-presenting cells. When its extracellular domain binds to an unidentified ligand of activated T cells, the T cell is silenced. Our objective was to study the expression of ILT3 on circulating monocytes in RRMS. Freshly isolated peripheral blood mononuclear cells were analyzed by multicolored flow cytometry. The proportion of ILT3+CD14+ monocytes in blood, and ILT3 levels expressed by them, is lower in untreated multiple sclerosis in relapse than in: (1) untreated multiple sclerosis in remission (p < 0.009); (2) stable interferon β-treated relapsing—remitting multiple sclerosis (p < 0.001) and; (3) healthy controls (p < 0.009). Glatiramer acetate-stimulated CD4 + T cells, co-cultured with freshly isolated monocytes, proliferate significantly better (p = 0.0017 for multiple sclerosis; p = 0.0015 for controls) when T cell interaction with monocyte-expressed ILT3 is blocked by anti-ILT3 antibody. Interferon β is beneficial in multiple sclerosis; why so remains unclear. Interferon β-1b markedly increases ILT3 expression in vitro by monocytes from multiple sclerosis patients and controls. These findings identify a putative novel mechanism for the therapeutic benefit bestowed by Interferon β and a new target for therapeutic intervention in relapsing—remitting multiple sclerosis.

Defining the response to interferon‐β in relapsing‐remitting multiple sclerosis patients

2006 ◽  
Vol 59 (2) ◽  
pp. 344-352 ◽  
Author(s):  
Jordi Río ◽  
Carlos Nos ◽  
Mar Tintoré ◽  
Nieves Téllez ◽  
Ingrid Galán ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Interferon Β ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Multiple Sclerosis Patients ◽  
Relapsing Remitting Multiple Sclerosis

Argentinean recommendations on the identification of treatment failure in relapsing remitting multiple sclerosis patients

2018 ◽  
Vol 385 ◽  
pp. 217-224 ◽  
Author(s):  
Edgardo Cristiano ◽  
Ricardo Alonso ◽  
Amelia Alvez Pinheiro ◽  
Elizabeth A. Bacile ◽  
María Eugenia Balbuena ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Treatment Failure ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Multiple Sclerosis Patients ◽  
Relapsing Remitting Multiple Sclerosis

Predicting beta-interferon failure in relapsing-remitting multiple sclerosis

2007 ◽  
Vol 13 (3) ◽  
pp. 336-342 ◽  
Author(s):  
K. O'Rourke ◽  
C. Walsh ◽  
G. Antonelli ◽  
M. Hutchinson
Keyword(s):  
Multiple Sclerosis ◽  
Treatment Failure ◽  
Failure Criteria ◽  
Control Group ◽  
Beta Interferon ◽  
Disability Status ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Relapsing Remitting Multiple Sclerosis

Proposed beta-interferon (IFNβ) treatment failure criteria for patients with relapsing-remitting multiple sclerosis (RRMS) have not been validated in clinical practice. This study aimed to establish (a) whether IFNβ attenuated accumulation of fixed disability in comparison to a cohort of matched historical control subjects from the Sylvia Lawry centre for MS research, and (b) whether relapse-based treatment failure criteria or clinical and demographic variables had predictive value for the accumulation of fixed disability. Of the 175 IFNβ-treated RRMS patients, 60 (34%) developed accumulation of fixed disability over a median of five years follow-up, which was significantly less than the rate of accumulation of fixed disability in the control group (P<0.0001). Any relapse in the treatment period predicted accumulation of fixed disability with a sensitivity of 80% and specificity of 43%; patients totally relapse free were less likely to develop accumulation of fixed disability (P <0.002). Multivariate analysis confirmed that a greater risk of accumulation of fixed disability was conferred by a higher Expanded Disability Status Scale (EDSS) score starting IFNβ (P=0.02), and by failure of IFNβ to completely suppress relapses (P=0.004). In conclusion, IFNβ therapy reduced the accumulation of fixed disability in a cohort of RRMS patients, followed for a median of five years. Higher baseline EDSS and failure of complete relapse suppression were associated with a significantly greater likelihood of accumulation of fixed disability. Multiple Sclerosis 2007; 13: 336-342. http://msj.sagepub.com

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