Single-cell profiling reveals preferential reduction of memory B cell subsets in cladribine patients that correlates with treatment response.

cladribine memory B cells multiple sclerosis

Journal

Therapeutic advances in neurological disorders
ISSN: 1756-2856
Titre abrégé: Ther Adv Neurol Disord
Pays: England
ID NLM: 101480242

Informations de publication

Date de publication:
2023
Historique:
received: 14 06 2023
accepted: 14 10 2023
medline: 12 12 2023
pubmed: 12 12 2023
entrez: 12 12 2023
Statut: epublish

Résumé

Cladribine is a highly effective immunotherapy that is applied in two short-term courses over 2 years and reduces relapse rate and disease progression in patients with relapsing multiple sclerosis (MS). Despite the short treatment period, cladribine has a long-lasting effect on disease activity even after recovery of lymphocyte counts, suggesting a yet undefined long-term immune modulating effect. Our aim was to provide a more profound understanding of the detailed effects of cladribine, also with regard to the patients' therapy response. We performed an open-labeled, explorative, prospective, single-arm study, in which we examined the detailed lymphocyte subset development of MS patients who received cladribine treatment over 2 years. We performed in-depth profiling of the effects of cladribine on peripheral blood lymphocytes by flow cytometry, bulk RNA sequencing of sorted CD4 Flow cytometry revealed a predominant and sustained reduction of memory B cells compared to other B cell subsets after cladribine treatment, whereas T cell subsets were slightly reduced in a more uniform pattern. The overall transcriptional profile of total blood B cells exhibited reduced expression of proinflammatory and T cell activating genes, while single-cell transcriptomics revealed that gene expression within each B cell cluster did not change over time. Stable patients displayed stronger reductions of selected memory B cell clusters as compared to patients with clinical or cerebral MRI disease activity. We describe a pronounced and sustained effect of cladribine on the memory B cell compartment, and the resulting change in B cell subset composition causes a significant alteration of B cell transcriptional profiles resulting in reduced proinflammatory and T cell activating capacities. The extent of reduction in selected memory B cell clusters by cladribine may predict treatment response.

Sections du résumé

Background UNASSIGNED
Cladribine is a highly effective immunotherapy that is applied in two short-term courses over 2 years and reduces relapse rate and disease progression in patients with relapsing multiple sclerosis (MS). Despite the short treatment period, cladribine has a long-lasting effect on disease activity even after recovery of lymphocyte counts, suggesting a yet undefined long-term immune modulating effect.
Objectives UNASSIGNED
Our aim was to provide a more profound understanding of the detailed effects of cladribine, also with regard to the patients' therapy response.
Design UNASSIGNED
We performed an open-labeled, explorative, prospective, single-arm study, in which we examined the detailed lymphocyte subset development of MS patients who received cladribine treatment over 2 years.
Methods UNASSIGNED
We performed in-depth profiling of the effects of cladribine on peripheral blood lymphocytes by flow cytometry, bulk RNA sequencing of sorted CD4
Results UNASSIGNED
Flow cytometry revealed a predominant and sustained reduction of memory B cells compared to other B cell subsets after cladribine treatment, whereas T cell subsets were slightly reduced in a more uniform pattern. The overall transcriptional profile of total blood B cells exhibited reduced expression of proinflammatory and T cell activating genes, while single-cell transcriptomics revealed that gene expression within each B cell cluster did not change over time. Stable patients displayed stronger reductions of selected memory B cell clusters as compared to patients with clinical or cerebral MRI disease activity.
Conclusion UNASSIGNED
We describe a pronounced and sustained effect of cladribine on the memory B cell compartment, and the resulting change in B cell subset composition causes a significant alteration of B cell transcriptional profiles resulting in reduced proinflammatory and T cell activating capacities. The extent of reduction in selected memory B cell clusters by cladribine may predict treatment response.

Identifiants

pubmed: 38084102
doi: 10.1177/17562864231211077
pii: 10.1177_17562864231211077
pmc: PMC10710756
doi:

Types de publication

Journal Article

Langues

eng

Pagination

17562864231211077

Informations de copyright

© The Author(s), 2023.

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Auteurs

Valerie E Teschner (VE)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Ann-Katrin Fleck (AK)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Carolin Walter (C)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.
Institute of Medical Informatics, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Anna-Sophie Schwarze (AS)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Melanie Eschborn (M)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Timo Wirth (T)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Olga V Steinberg (OV)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Andreas Schulte-Mecklenbeck (A)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

I-Na Lu (IN)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Marisol Herrera-Rivero (M)

Department of Genetic Epidemiology, Institute of Human Genetics, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Claudia Janoschka (C)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Jan D Lünemann (JD)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Nicholas Schwab (N)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Gerd Meyer Zu Hörste (G)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Julian Varghese (J)

Institute of Medical Informatics, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Catharina C Gross (CC)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Refik Pul (R)

Department of Neurology, Universität Duisburg-Essen, Essen, Germany.

Christoph Kleinschnitz (C)

Department of Neurology, Universität Duisburg-Essen, Essen, Germany.

Simone Mader (S)

Institute of Clinical Neuroimmunology, Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München, München, Germany.

Edgar Meinl (E)

Institute of Clinical Neuroimmunology, Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München, München, Germany.

Monika Stoll (M)

Department of Genetic Epidemiology, Institute of Human Genetics, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Heinz Wiendl (H)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany.

Luisa Klotz (L)

Department of Neurology with Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Albert-Schweitzer-Campus 1, Münster 48149, Germany.

Classifications MeSH