Multiple Sclerosis, Neuroimmunology CE/CME ACCREDITED Watch Time: 31 mins

touchTALKS Understanding the pathophysiology of multiple sclerosis and the development of new therapies

Prof. Tobias Derfuss reviews the cellular model of disease in multiple sclerosis, and how pathophysiology can offer novel therapeutic targets.

Video Chapters
The role of immune cells in MS pathogenesis

Prof. Tobias Derfuss outlines the cellular model of multiple sclerosis, including the role of immune cells in disease pathogenesis.

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Pathogenic mechanisms as therapeutic targets

Prof. Tobias Derfuss reviews the available disease-modifying therapies for multiple sclerosis and how their mechanisms of action target the pathobiology of the disease.

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A new therapeutic target: Bruton’s tyrosine kinase

Prof. Tobias Derfuss discusses the mechanism of action and the latest clinical trial data for Bruton’s tyrosine kinase inhibitors.

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Overview & Learning Objectives

In this activity, Prof. Tobias Derfuss outlines the role of immune cells in driving multiple sclerosis pathogenesis, explains how the pathobiology of the disease has driven the development of disease-modifying therapies, and reviews the mechanism of action and clinical trial landscape for Bruton’s tyrosine kinase inhibitors.

This activity is jointly provided by USF Health and touchIME. read more

Target Audience

This activity has been designed to meet the educational needs of general neurologists, MS specialists and MS nurses involved in the management of multiple sclerosis.


USF Health adheres to the Standards for Integrity and Independence in Accredited Continuing Education. All individuals in a position to influence content have disclosed to USF Health any financial relationship with an ineligible organization. USF Health has reviewed and mitigated all relevant financial relationships related to the content of the activity. The relevant relationships are listed below. All individuals not listed have no relevant financial relationships.


Prof. Tobias Derfuss discloses: Consultancy fees from Alexion, Biogen, Celgene, GeNeuro, MedDay, Merck, Novartis, and Sanofi. Grant/research support from Merck, Novartis, and Roche.

Content reviewer

Niraja S. Suresh, MD discloses: Advisory board or panel fees from Alexion, Alnylam Pharmaceuticals, Argenx, (relationships terminated) and Collegium Pharmaceutical. Speakers’ Bureau fees from Takeda.

Touch Medical Director

Holly Gilbert-Jones and Kathy Day have no financial interests/relationships or affiliations in relation to this activity.

USF Health Office of Continuing Professional Development and touchIME staff have no financial interests/relationships or affiliations in relation to this activity.

Requirements for Successful Completion

In order to receive credit for this activity, participants must review the content and complete the post-test and evaluation form. Statements of credit are awarded upon successful completion of the post-test and evaluation form.

If you have questions regarding credit please contact 



This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through a joint providership of USF Health and touchIME. USF Health is accredited by the ACCME to provide continuing medical education for physicians.

USF Health designates this enduring material for a maximum of 0.75 AMA PRA Category 1 CreditTM.  Physicians should claim only the credit commensurate with the extent of their participation in the activity.

The European Union of Medical Specialists (UEMS) – European Accreditation Council for Continuing Medical Education (EACCME) has an agreement of mutual recognition of continuing medical education (CME) credit with the American Medical Association (AMA). European physicians interested in converting AMA PRA Category 1 CreditTM into European CME credit (ECMEC) should contact the UEMS (

Advanced Practice Providers

Physician Assistants may claim a maximum of 0.75 Category 1 credits for completing this activity. NCCPA accepts AMA PRA Category 1 CreditTM from organizations accredited by ACCME or a recognized state medical society.

The AANPCP accepts certificates of participation for educational activities approved for AMA PRA Category 1 CreditTM by ACCME-accredited providers. APRNs who participate will receive a certificate of completion commensurate with the extent of their participation.

Date of original release: 13 March 2023. Date credits expire: 13 March 2024.

If you have any questions regarding credit please contact

Learning Objectives

After watching this activity, participants should be better able to:

  • Explain the cellular model of disease in multiple sclerosis
  • Explain how the pathobiology of multiple sclerosis drives the development of disease-modifying therapies
  • Summarize the mechanism of action of Bruton’s tyrosine kinase inhibitors and how this may translate into clinical benefits for patients with multiple sclerosis
Faculty & Disclosures
Prof. Tobias Derfuss

University Hospital Basel, Switzerland

Prof. Tobias Derfuss is the head of the outpatient care unit and deputy head of the MS Center at the Department of Neurology, University Hospital Basel, Switzerland, and research group leader in clinical neuroimmunology at the Department of Biomedicine at the University of Basel. read more

He is a clinical neurologist, specializing in neuroimmunology. Prof. Derfuss undertook his clinical training at the Department of Neurology, Klinikum Grosshadern in Munich, Germany. His research at the Max-Planck Institute for Neurobiology, Department of Neuroimmunology, was focused on the discovery of new autoantigens in multiple sclerosis (MS) and the characterization of the immune response against latent herpes viruses. After training in neuromuscular diseases at the Friedrich-Baur Institute and in psychiatry at the Max-Planck Institute for Psychiatry in Munich, he was appointed head of the outpatient department and MS clinic in the Department of Neurology at the University Hospital Erlangen in 2009.

Since 2010, he has been professor and senior physician at the Department of Neurology and research group leader at the Department of Biomedicine at the University Hospital Basel. His main research focus is the discovery of biomarkers and analysing the mode of action of disease-modifying treatments in neuroinflammatory diseases. Prof. Derfuss is also involved in the design and conduct of clinical trials for newly emerging therapies in MS.

Prof. Tobias Derfuss discloses: Consultancy fees from Alexion, Biogen, Celgene, GeNeuro, MedDay, Merck, Novartis and Sanofi. Grants/research support from Merck, Novartis and Roche.

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Question 1/5
Which of the following cells are required to interact with B cells to allow them to develop into T-bet-expressing memory cells?

CD, cluster of differentiation; T-bet, T-box expressed in T cells; Th, T helper; Treg, regulatory T cell.

Once activated B cells enter the germinal centres they interact with CD4 Th cells via CD40 and HLA-II. With additional influence of IFN-γ and IL-21, they develop into T-bet-expressing memory cells.


CD, cluster of differentiation; HLA, human leucocyte antigen; IFN, interferon; IL, interleukin; T-bet, T-box expressed in T cells; Th, T helper.

van Langelaar J, et al. Front Immunol. 2020;11:760.

Question 2/5
Your patient with relapsing MS starts on treatment with the purine analogue, cladribine. Based on recent data, which of the following outcomes would you expect over 12 months after the first course of tablets?

MS, multiple sclerosis.

The MAGNIFY-MS substudy investigated the changes in cell subtypes over 12 months after the first course of cladribine tablets in patients with highly active relapsing MS. Study investigators reported that naive B cells recovered toward baseline, CD4 and CD8 T cells recovered but to levels below baseline, and memory B cells remained depleted until month 12.


CD, cluster of differentiation; MS, multiple sclerosis.


Wiendl H, et al. Neurol Neuroimmunol Neuroinflamm. 2023;10:e200048.

Question 3/5
Your patient with highly relapsing MS starts on treatment with the immune cell migration inhibitor, natalizumab. Which of the following treatment effects would you expect?

MS, multiple sclerosis.

Natalizumab blocks the binding of lymphocytes to VCAM-1 expressed on endothelial cells and prevents their entry into the central nervous system.1 This increases the number of lymphocytes in the blood.2


VCAM-1, vascular cell adhesion protein 1.


  1. Steinman L. J Cell Biol. 2012;199:413–6.
  2. Plavina T, et al. Neurology. 2017;89:1584–93.
Question 4/5
Your patient with MS has had three relapses in the past 2 years, two of which have occurred within the past year and one active gadolinium-enhancing brain lesion in the last 6 months. Assuming future approval, you decide to initiate treatment with a BTK inhibitor. What is your rationale for selecting this class of agent?

BTK, Bruton's tyrosine kinase; MS, multiple sclerosis.

Following the binding of antigen to the BCR, activation of BTK leads to downstream inhibition of two pathways that regulate the gene expression required for B-cell proliferation, maturation, differentiation and chemokine/cytokine expression.


BCR, B-cell receptor; BTK, Bruton’s tyrosine kinase.


Jayagopal JA, Zabad RK. 2022. Available at: (accessed 20 February 2023).

Question 5/5
Your patient has relapsing MS and an EDSS score of 5. You consider enrolling the patient in a clinical trial with the BTK inhibitor, evobrutinib. When discussing this course of action with your patient, which of the following efficacy outcomes would you highlight as being associated with phase II data?

BTK, Bruton’s tyrosine kinase; EDSS, Expanded Disability Status Scale; MS, multiple sclerosis.

A randomized phase II trial investigating evobrutinib vs dimethyl fumerate reported that the mean (±SD) total number of gadolinium-enhancing lesions at weeks 12 through 24 was lower in the evobrutinib groups (4.06±8.02, 1.69±4.69 and 1.15±3.70 for 25 mg QD, 75 mg QD and 75 mg BID, respectively) compared with the dimethyl fumerate group (4.78±22.05).


BID, twice daily; QD, once daily; SD, standard deviation.


Montalban X, et al. N Engl J Med. 2019;380:2406–17.

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