MS Inside Out means exploring innovative pathways

We work collaboratively to discover and deliver transformative treatments that significantly improve the lives of people living with chronic progressive diseases, especially those of the immune system.

We are discovering new ways to optimize outcomes for a range of chronic progressive diseases by pursuing novel pathways that modulate the immune system in more targeted manners than traditional immunosuppressants.

For immune disorders, we develop approaches that target the innate and adaptive components of the immune system. This includes inhibiting the inappropriate immune activation that contributes to the disorder, as well as inducing immune tolerance, which trains the body not to react to triggers.  

To continue discovering and delivering best-in-class therapies for patients, we believe it is crucial to pair our diverse internal expertise with strategic external partnerships.

• This strategy has enabled us to work alongside leading academic institutions and innovative companies to pursue research in new areas and uncover potential therapies.
• Together, we can achieve our goals faster and smarter, to ultimately create a future where patients with chronic progressive diseases can live disease-free. 

Understanding how the innate and adaptive immune systems communicate through different players may help deepen our understanding of what causes MS and what perpetuates the disease. Lymphocytes play a central role, with B and T cell subsets each contributing to the disease in their own way.^1-4

The lymphocyte subsets below are considered to be key drivers of continued neuroinflammation in MS. Elaborate communication between lymphocytes activates and perpetuates the inflammatory cascade. Lymphocytes do not act alone; they use crosstalk to stimulate each other. Clonal expansion occurs in the periphery, and on re-exposure to antigens, memory B and T cells respond more robustly and rapidly.^5-8

Naive B cell
Cells that, when activated by antigen and helper T cells, differentiate into memory B cells or plasma cells which produce and secrete antibodies with a unique antigen-binding site⁷ 

Memory B cell

Cells that form from naive B cells on initial antigen exposure and—when activated by the antigen with the aid of a helper T cell—more rapidly proliferate and differentiate into antibody-secreting plasma cells^7,9

Naive helper T cell
Type of T cell that can activate a B cell once it is activated by an antigen-presenting cell⁷

Memory helper T cell
Helper T cells, once activated by antigen-presenting cells, that will activate the immune response more rapidly upon antigen re-exposure⁹

CD8 cytotoxic naive T cell
Cytotoxic cells that will assist in the elimination of antigenic cells, but have not yet been exposed to antigen¹⁰

CD8 cytotoxic memory T cell
Memory T cells that respond robustly and quickly on re-exposure to antigens by rapidly re-expressing effector molecules, such as cytokines and proteins of the lytic machinery¹⁰

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1. Salou M, Nicol B, Garcia A, Laplaud DA . Involvement of CD8+ T cells in multiple sclerosis. Front Immunol. 2015;6: 604. 

2. Bittner S, Ruck T, Wiendl H, Grauer OM, Meuth SG. Targeting B cells in relapsing–remitting multiple sclerosis: from pathophysiology to optimal clinical management. Ther Adv Neurol Disord. 2017;10:51-66. 

3. Baker D, Marta M, Pryce G, Giovannoni G, Schmierer K. Memory B cells are major targets for effective immunotherapy in relapsing multiple sclerosis. EBioMedicine. 2017;16:41-50. 

4. Li R, Rezk A, Healy LM, et al. Cytokine-defined B cell responses as therapeutic targets in multiple sclerosis. Front Immunol. 2015;6:626. 

5. Paroni M, Maltese V, De Simone M, et al. Recognition of viral and self-antigens by TH1 and TH1/TH17 central memory cells in patients with multiple sclerosis reveals distinct roles in immune surveillance and relapses. J Allergy Clin Immunol. 2017;140:797-808. 

6. Mitsdoerffer M, Peters A. Tertiary lymphoid organs in central nervous system autoimmunity. Front Immunol. 2016;7:451. 

7. Dalakas M. B cells as therapeutic targets in autoimmune neurological disorders. Nat Clin Pract Neurol. 2008;4:557-567. 

8. Pikor N, Prat A, Bar-Or A, Gommerman J. Meningeal tertiary lymphoid tissues and multiple sclerosis: a gathering place for diverse types of immune cells during CnS autoimmunity. Front Immunol. 2016;6:1-7.

9. Fan X, Jin T, Zhao S, et al. Circulating CCR7+ ICOS+ memory T follicular helper cells in patients with multiple sclerosis. PLoS One. 2015;10(7):e0134523.

10. Liu G, Fang LB, Hjelmström, Gao XG. Increased CD8+ central memory T cells in patients with multiple sclerosis. Mult Scler. 2007;13:149-155.