This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
Abstract
Multiple sclerosis (MS) is a debilitating autoimmune disease characterized by both inflammation and axonal degeneration. The resulting demyelination and subsequent degeneration of axons account for the disability of patients with MS. Early investigations indicated that disease progression was driven by CD4+ effector T cells. However, clinical therapies specifically targeting these cells have, for the most part, not been effective. Therefore, new areas of research in experimental autoimmune encephalomyelitis (the experimental model of MS) and human MS have identified previously unknown contributions to disease pathogenesis, including interleukin-17-producing T helper 17 cells, B cells, CD8+ T cells, and both CD4+ and CD8+ T-regulatory cells. Research into the respective mechanisms of action of these cells has identified novel therapeutic targets to combat this devastating disease. This article reviews the autoimmune response in patients with MS compared with individuals without MS and summarizes the fundamental differences in the immunologic response between people with and without MS. Investigations into these autoimmune differences and the disruption of the homeostatic balance of the immune system will help guide future research into MS therapeutics, with particular attention to the long-term management of this disease.
Glossary
- AIS=
- adaptive immune system;
- APC=
- antigen-presenting cells;
- BAFF=
- B-cell-activating factor;
- CSF=
- cerebral spinal fluid;
- DC=
- dendritic cell;
- EAE=
- experimental autoimmune encephalomyelitis;
- IFN=
- interferon;
- IL=
- interleukin;
- MHC=
- major histocompatibility complex;
- MS=
- multiple sclerosis;
- MyD=
- myeloid differentiation factor;
- NK=
- natural killer;
- T regs=
- T-regulatory cells;
- TCR=
- T-cell receptor;
- TGF=
- transforming growth factor;
- Th=
- T helper;
- TLR=
- toll-like receptor.
AAN Members
We have changed the login procedure to improve access between AAN.com and the Neurology journals. If you are experiencing issues, please log out of AAN.com and clear history and cookies. (For instructions by browser, please click the instruction pages below). After clearing, choose preferred Journal and select login for AAN Members. You will be redirected to a login page where you can log in with your AAN ID number and password. When you are returned to the Journal, your name should appear at the top right of the page.
AAN Non-Member Subscribers
Purchase access
Letters: Rapid online correspondence
REQUIREMENTS
You must ensure that your Disclosures have been updated within the previous six months. Please go to our Submission Site to add or update your Disclosure information.
Your co-authors must send a completed Publishing Agreement Form to Neurology Staff (not necessary for the lead/corresponding author as the form below will suffice) before you upload your comment.
If you are responding to a comment that was written about an article you originally authored:
You (and co-authors) do not need to fill out forms or check disclosures as author forms are still valid
and apply to letter.
Submission specifications:
- Submissions must be < 200 words with < 5 references. Reference 1 must be the article on which you are commenting.
- Submissions should not have more than 5 authors. (Exception: original author replies can include all original authors of the article)
- Submit only on articles published within 6 months of issue date.
- Do not be redundant. Read any comments already posted on the article prior to submission.
- Submitted comments are subject to editing and editor review prior to posting.
