New Research Highlights Pathogenic Role of B Cells in Multiple Sclerosis

While T cells have been known to play a role in the pathogenesis of multiple sclerosis (MS), new research indicates that T cell interactions with B cells may drive inflammation and brain lesions in the disease, according to a new study published in Cell.
In patients with MS, disrupted T cells attack and damage the body’s myelin sheaths that surround nerve cells in the brain and spinal cord, affecting their ability to communicate with each other. The new findings suggest that B cells, the cells that produce antibodies, also play a key role in causing the onset of MS by activating the specific T cells that cause inflammation in the brain and nerve cell lesions.
The findings provide an explanation for how new MS drugs take effect, according to researchers from the University of Zurich. Certain drugs used to treat MS, such as Rituximab and Ocrelizumab, eliminate B cells to effectively inhibit brain inflammation and flare-ups. This novel approach led the researchers to believe that B cell interaction with T cells may be a key factor in the development of the disease, an understanding that could lead to new approaches in the treatment of MS.
“This means that we can now explain the previously unclear mechanism of these MS drugs,” Roland Martin, MD, director of Clinical Research Priority Program Multiple Sclerosis at University of Zurich, said in a press release.
By using an experimental in-vitro system, the researchers analyzed blood samples of patients with MS to establish the B cells’ role. When the B cells interacted with the T cells, the blood of patients with MS showed increased levels of activation and cellular division among T cells attacking the body’s myelin sheaths that surround nerve cells. The researchers found that when the B cells were eliminated, the proliferation of T cells was effectively inhibited.
Additionally, the activated T cells found in the blood included those that also occur in the brain in patients during flare-ups of the disease. Once the T cells are activated in the peripheral blood, they migrate to the brain.
“These findings will be instrumental to address important questions regarding pathogenic B-T cells interactions in multiple sclerosis and possibly also to develop novel therapies,” the researchers concluded in the study.  
Jelcic I, Nimer FA, Wang J, et al. Memory B cells activate brain-homing, autoreactive CD4+ T cells in multiple sclerosis. Cell. 2018. Doi:
B Cells Among Factors Leading to Brain Lesions in Multiple Sclerosis [news release]. University of Zurich’s website. Accessed September 5, 2018.

Stay up to date on the latest news in specialty pharmacy by getting Specialty Pharmacy Times in your mailbox or inbox for free!

Click here to sign up for free for the bi-monthly Specialty Pharmacy Times print journal delivered to your address.

Click here to sign up for our email newsletters delivered every Monday, Wednesday, and Friday, in addition to breaking news alerts.

Click here to follow us on Facebook. 

Click here to follow us on Twitter. 

Click here to join our LinkedIn group. 

Related Articles

Selinexor (Xpovio, Karyopharm) received approval in combination with dexamethasone for heavily-pretreated patients with relapsed or refractory multiple myeloma.
Daratumumab (Darzalex, Janssen) is indicated for use in combination with lenalidomide and dexamethasone for patients with newly-diagnosed multiple myeloma who are ineligible for autologous stem cell transplant.
Top news of the day from across the health care landscape.
Company Profile >
Industry Guide >
Market News >
Peer Exchange >
Conferences >
Subscribe >
Specialty Times Resources
About Us
Contact Us
Terms & Conditions
MJH Associates >
Pharmacy Times
American Journal of Managed Care
MD Magazine
Targeted Oncology
Physicians' Education Resource
Pharmacy & Healthcare Communications, LLC
2 Clarke Drive
Suite 100
Cranbury, NJ 08512
P: 609-716-7777
F: 609-716-4747

Copyright Specialty Pharmacy Times 2006-2019
Pharmacy & Healthcare Communications, LLC. All Rights Reserved.