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Alemtuzumab differentially affects effector and regulatory immune cell subsets
Author(s): ,
S. Palmeri
Affiliations:
Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova
,
F. Ivaldi
Affiliations:
Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova
,
C. Lapucci
Affiliations:
Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova
,
G.L. Mancardi
Affiliations:
Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova; University of Genova, IRCCS AOU San Martino-IST, Genova, Italy
,
N. Kerlero de Rosbo
Affiliations:
Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova
,
A. Uccelli
Affiliations:
Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova; University of Genova, IRCCS AOU San Martino-IST, Genova, Italy
A. Laroni
Affiliations:
Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova; University of Genova, IRCCS AOU San Martino-IST, Genova, Italy
ECTRIMS Online Library. Palmeri S. Oct 12, 2018; 229046
Serena Palmeri
Serena Palmeri
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Abstract: P1206

Type: Poster Sessions

Abstract Category: Therapy - Immunomodulation/Immunosuppression

Introduction: Alemtuzumab is an anti-CD52 human monoclonal antibody approved for the treatment of MS. Alemtuzumab causes a transient decrease in immune cell subsets followed by repopulation. Differential targeting of immune cells may be associated to its efficacy and/or side effects, including a 30% risk in secondary autoimmune diseases.
Objectives: To ascertain the effect of alemtuzumab on the phenotype of immune cells.
Aims:
1. To study how alemtuzumab affects the absolute number (AN) of main immune cell subsets.
2. To study how alemtuzumab affects the proportion of 21 effector and regulatory immune cell subsets belonging to the adaptive and innate immune system.
Methods: AN of B, T and NK cells over the first year of treatment were evaluated by conventional flow cytometry (N=14 patients). In order to measure the proportion of effector and regulatory T, B and NK cell subsets over treatment, a highly standardized method for flow cytometry, using tubes pre-filled with lyophilized fluorescent antibodies (Lyotubes), was employed in a subset of patients.
Results: Immediate post-treatment (PT) decrease in AN of all immune cell subsets was observed compared to baseline. At subsequent time-points, AN of CD3+ T cells were persistently decreased; AN of CD19 + B cells were increased at 12 months PT; AN of NK cells were unchanged. Through highly standardized flow cytometry, we observed a trend to an increase in Th1 cells at 3 months PT; total T regulatory cells were persistently decreased PT. Proportions of B regulatory and B memory cells increased 3 months PT. CD56brightNK cells increased in half subjects PT.
Conclusions: Alemtuzumab differentially affects immune effector and regulatory immune cell subsets.
Disclosure: S. Palmeri: nothing to disclose. F. Ivaldi: nothing to disclose. C. Lapucci has received travel funds from Roche. G. Mancardi has received honoraria, travel expenses, and financial support for research from Biogen, Bayer Schering, Sanofi Aventis, Teva, Merck-Serono, and Novartis. N. Kerlero de Rosbo: nothing to disclose. A. Uccelli has received consulting honoraria and/or speaker fees from Genentech, Roche, Biogen, Genzyme, Teva, Novartis, and Merck-Serono. A. Laroni has received personal compensation from Novartis, Genzyme, Biogen, Merck and TEVA for public speaking and/or advisory boards.

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