Neutralizing antibodies explain the poor clinical response to Interferon beta in a small proportion of patients with Multiple Sclerosis: a retrospective study

doi:10.1186/1471-2377-9-54

BMC Neurology
Volume 9

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Sbardella E
Tomassini V
Gasperini C
Bellomi F
Cefaro LA
Morra VB
Antonelli G
Pozzilli C

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Tomassini V
Gasperini C
Bellomi F
Cefaro LA
Morra VB
Antonelli G
Pozzilli C
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Research article

Neutralizing antibodies explain the poor clinical response to Interferon beta in a small proportion of patients with Multiple Sclerosis: a retrospective study

Emilia Sbardella¹ , Valentina Tomassini¹^,2 , Claudio Gasperini³ , Francesca Bellomi⁴ , Luca Ausili Cefaro¹ , Vincenzo Brescia Morra⁵ , Guido Antonelli⁴ and Carlo Pozzilli¹

¹Departments of Neurological Sciences, "Sapienza" University, Rome, Italy

²FMRIB Centre, The University of Oxford, Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK

³Department of Neurology, San Camillo Hospital, Rome, Italy

⁴Experimental Medicine and Pathology, Section of Virology, "Sapienza" University, Rome, Italy

⁵Department of Neurological Sciences, "Federico II" University, Naples, Italy

author email corresponding author email

BMC Neurology 2009, 9:54doi:10.1186/1471-2377-9-54


Published:	13 October 2009

Abstract

Background

Neutralizing antibodies (NAbs) against Interferon beta (IFNβ) are reported to be associated with poor clinical response to therapy in multiple sclerosis (MS) patients. We aimed to quantify the contribution of NAbs to the sub-optimal response of IFNβ treatment.

Methods

We studied the prevalence of NAbs in MS patients grouped according to their clinical response to IFNβ during the treatment period. Patients were classified as: group A, developing ≥ 1 relapse after the first 6 months of therapy; group B, exhibiting confirmed disability progression after the first 6 months of therapy, with or without superimposed relapses; group C, presenting a stable disease course during therapy. A cytopathic effect assay tested the presence of NAbs in a cohort of ambulatory MS patients treated with one of the available IFNβ formulations for at least one year. NAbs positivity was defined as NAbs titre ≥ 20 TRU.

Results

Seventeen patients (12.1%) were NAbs positive. NAbs positivity correlated with poorer clinical response (p < 0.04). As expected, the prevalence of NAbs was significantly lower in Group C (2.1%) than in Group A (17.0%) and Group B (17.0%). However, in the groups of patients with a poor clinical response (A, B), NAbs positivity was found only in a small proportion of patients.

Conclusion

The majority of patients with poor clinical response are NAbs negative suggesting that NAbs explains only partially the sub-optimal response to IFNβ.