The chemokine receptor CCR5 Δ32 allele in natalizumab-treated multiple sclerosis

Authors

  • M. Møller,

    1. Department of Neurology, The Danish Multiple Sclerosis Center, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark
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  • H. B. Søndergaard,

    1. Department of Neurology, The Danish Multiple Sclerosis Center, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark
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  • N. Koch-Henriksen,

    1. Danish Multiple Sclerosis Treatment Registry, Rigshospitalet, Copenhagen, Denmark
    2. Department of Neurology, University Hospital in Aalborg, Aalborg, Denmark
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  • P. S. Sorensen,

    1. Department of Neurology, The Danish Multiple Sclerosis Center, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark
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  • F. Sellebjerg,

    Corresponding author
    1. Department of Neurology, The Danish Multiple Sclerosis Center, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark
    • F. Sellebjerg, The Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark

      Tel.: +45 3545 2280

      Fax: +45 3545 2626

      e-mail: sellebjerg@dadlnet.dk

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  • A. B. Oturai

    1. Department of Neurology, The Danish Multiple Sclerosis Center, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark
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Abstract

Objective

The chemokine receptor CCR5 may be important for the recruitment of pathogenic T cells to the CNS in multiple sclerosis (MS). We hypothesized that this chemokine receptor might still be important for T-cell migration during treatment with anti-very late antigen (VLA)-4 antibody. We therefore analysed whether natalizumab-treated MS patients carrying the CCR5 Δ32 deletion allele, which results in reduced expression of CCR5 on the cell surface, had lower disease activity.

Methods

CCR5 Δ32 was analysed in 212 natalizumab-treated MS patients.

Results

CCR5 Δ32 status had no significant impact on the frequency of relapses 1 year prior to natalizumab treatment or during the first 48 weeks of treatment. The multiple sclerosis severity score (MSSS) was significantly lower at baseline in patients carrying CCR5 Δ32 (P = 0.031).

Conclusions

CCR5 Δ32 is not associated with lower disease activity in MS patients treated with natalizumab. We found lower MSSS scores in patients carrying CCR5 Δ32 compared with the remaining patients, which is consistent with previous studies reporting an association with a more favourable disease course. Further studies are, however, needed before the relationship between CCR5 Δ32 and disease activity in MS can be definitely established.

Ancillary