Editing Multiple sclerosis (section)

=== Immune dysregulation ===
As briefly detailed in the [[Multiple sclerosis#Immune dysregulation|causes section]] of this article, MS is currently thought to stem from a failure of the body's immune system to kill off autoreactive T-cells & B-cells.<ref name="Ward 988–1005"/> Currently, the T-cell subpopulations that are thought to drive the development of MS are autoreactive CD8+ T-cells, CD4+ helper T-cells, and T<sub>H</sub>17 cells. These autoreactive T-cells produce substances called [[cytokine]]s that induce an inflammatory immune response in the CNS, leading to the development of the disease.<ref name="Ward 988–1005"/> More recently, however, the role of autoreactive B-cells has been elucidated. Evidence of their contribution to the development of MS is implicated through the presence of [[oligoclonal bands|oligoclonal IgG bands]] (antibodies produced by B-cells) in the [[cerebrospinal fluid|CSF]] of patients with MS.<ref name="Ward 988–1005"/><ref name="McGinley_2021"/> The presence of these oligoclonal bands has been used as supportive evidence in clinching a diagnosis of MS.<ref name="Thompson-2018">{{cite journal | vauthors = Thompson AJ, Banwell BL, Barkhof F, Carroll WM, Coetzee T, Comi G, Correale J, Fazekas F, Filippi M, Freedman MS, Fujihara K, Galetta SL, Hartung HP, Kappos L, Lublin FD, Marrie RA, Miller AE, Miller DH, Montalban X, Mowry EM, Sorensen PS, Tintoré M, Traboulsee AL, Trojano M, Uitdehaag BM, Vukusic S, Waubant E, Weinshenker BG, Reingold SC, Cohen JA | title = Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria | journal = The Lancet. Neurology | volume = 17 | issue = 2 | pages = 162–173 | date = February 2018 | pmid = 29275977 | doi = 10.1016/s1474-4422(17)30470-2 | url = https://discovery.ucl.ac.uk/id/eprint/10041020/ | archive-date = 28 May 2023 | access-date = 20 January 2024 | archive-url = https://web.archive.org/web/20230528035839/https://discovery.ucl.ac.uk/id/eprint/10041020/ | url-status = live }}</ref> As similarly described before, B-cells can also produce cytokines that induce an inflammatory immune response via activation of autoreactive T-cells.<ref name="Ward 988–1005"/><ref>{{cite journal | vauthors = Hassani A, Reguraman N, Shehab S, Khan G | title = Primary Peripheral Epstein-Barr Virus Infection Can Lead to CNS Infection and Neuroinflammation in a Rabbit Model: Implications for Multiple Sclerosis Pathogenesis | journal = Frontiers in Immunology | volume = 12 | pages = 764937 | date = 2021 | pmid = 34899715 | pmc = 8656284 | doi = 10.3389/fimmu.2021.764937 | doi-access = free }}</ref> As such, higher levels of these autoreactive B-cells are associated with an increased number of lesions & neurodegeneration as well as worse disability.<ref name="Ward 988–1005"/>

Another cell population that is becoming increasingly implicated in MS is [[microglia]]. These cells are resident to & keep watch over the CNS, responding to pathogens by shifting between pro- & anti-inflammatory states. Microglia are involved in the formation of MS lesions and be involved in other diseases that primarily affect the CNS white matter. However, because of their ability to switch between pro- & anti-inflammatory states, microglia have also been shown to be able to assist in remyelination & subsequent neuron repair.<ref name="Ward 988–1005"/> As such, microglia are thought to be participating in both acute & chronic MS lesions, with 40% of [[phagocytic cell]]s in early active MS lesions being proinflammatory microglia.<ref name="Ward 988–1005"/>