In this paper, we use our unique tools to track autoimmune, and myelin T and B cells in a model of induced anti-myelin autoimmunity in mice. In human Multiple Sclerosis it has become apparent that B cells are very important players in promoting disease progression; in fact B cell targeting therapies have been approved for treatment of MS, including for the first time the progressive form of disease. However, we don’t know much about how these cells drive disease, and much of our research aims to figure this out.
B cells are known to invade the brains and spinal cords of people with MS, and they often form clusters with T cells adjacent to demyelinating lesions. Our initial assumption, based on what is known about the T cells that infiltrate the CNS in autoimmunity, was that many or even most of these B cells would be the ones that themselves target CNS autoantigen. We were surprised to find the opposite and that, if anything, activated autoimmune B cells are excluded from the inflamed CNS.
The usual caveat that this is a study in an animal disease model and not in human MS should be noted when interpreting findings from this paper. However, similar models of disease have previously revealed fundamental properties of the CNS/immune system relationship, and there is no reason to think that this is not the case here. Further, while some findings from human MS tissues have been interpreted to suggest B cells in the CNS are activated and target autoantigens, after closer reading of studies we are not convinced that this is the case. As with any study such as this, time will tell which is correct, but we will continue to address this issue in future studies.
Funding: This work in this paper was funded from an operating grant from the Canadian Institutes of Health Research (CIHR). Yodit’s stipend is funded from an Ontario Graduate Scholarship and Rajiv’s stipend is funded from a studentship from the MS Society of Canada. Please check out our funding page for more information.
A note about access: The conditions of our funding stipulate that publications must be freely accessible within a year of publication, and in accordance with this it will be possible to access the full and final version of this paper through the journal website within a year. Allowing early open access would have cost our research budget thousands of dollars over the ~$3000 CAD it already cost to publish this paper (lots of colour charges for pretty figures). If you want to read our paper but can’t get access, please contact us and we will do our best to get it to you.