B‐cell and T‐cell receptor repertoire in chronic inflammatory demyelinating polyneuropathy, a prospective cohort study

Author:

van Lieverloo G. G. A.1,Al‐Soudi A.23,Wieske L.1ORCID,Klarenbeek P. L.23,Anang D. C.23,Adrichem M. E.1,Niewold I.34,van Schaik B. D. C.5,van Kampen A. H. C.5,van Schaik I. N.1,de Vries N.23,Eftimov F.1

Affiliation:

1. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC University of Amsterdam Amsterdam The Netherlands

2. Department of Experimental Immunology, Amsterdam Infection & Immunity Institute, Amsterdam UMC University of Amsterdam Amsterdam The Netherlands

3. Department of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center (ARC) Amsterdam UMC Amsterdam The Netherlands

4. Amsterdam UMC Department of Genome Analysis Amsterdam The Netherlands

5. Amsterdam UMC, Department of Epidemiology & Data Science (EDS) Bioinformatics Laboratory Amsterdam The Netherlands

Abstract

AbstractThe immunopathophysiological mechanisms underlying chronic inflammatory demyelinating polyneuropathy (CIDP) in an individual patient are largely unknown. Better understanding of these mechanisms may aid development of biomarkers and targeted therapies. Both B‐ and T‐cell dominant mechanisms have been implicated. We therefore investigated whether B‐cell and T‐cell receptor (BCR/TCR) repertoires might function as immunological biomarkers in CIDP. In this prospective cohort study, we longitudinally sampled peripheral blood of CIDP patients in three different phases of CIDP: starting induction treatment (IT), starting withdrawal from IVIg maintenance treatment (MT), and patients in remission (R). BCR and TCR repertoires were analyzed using RNA based high throughput sequencing. In baseline samples, the number of total clones, the number of dominant BCR and TCR clones and their impact on the repertoire was similar for patients in the IT, MT, and remission groups compared with healthy controls. Baseline samples in the IT or MT did not predict treatment response or potential relapse at follow‐up. Treatment responders in the IT group showed a potential IVIg‐induced increase in the number of dominant BCR clones and their impact at follow‐up (baseline1.0 [IQR 1.0‐2.8] vs. 6 m 3.5 [0.3‐6.8]; P < .05, Wilcoxon test). Although the BCR repertoire changed over time, the TCR repertoire remained robustly stable. We conclude that TCR and BCR repertoire distributions do not predict disease activity, treatment response or response to treatment withdrawal.

Funder

Dutch Arthritis Association

Prinses Beatrix Spierfonds

ZonMw

Publisher

Wiley

Subject

Neurology (clinical),General Neuroscience

Reference37 articles.

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