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Autoimmunity
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== Low-level autoimmunity == While a high level of autoimmunity is unhealthy, a low level of autoimmunity may actually be beneficial. Taking the experience of a beneficial factor in autoimmunity further, one might hypothesize with intent to prove that autoimmunity is always a self-defense mechanism of the mammal system to survive. The system does not randomly lose the ability to distinguish between [[Self-protein|self]] and non-self; the attack on cells may be the consequence of cycling metabolic processes necessary to keep the blood chemistry in homeostasis.{{citation needed|date=June 2022}} Second, autoimmunity may have a role in allowing a rapid immune response in the early stages of an infection when the availability of foreign [[antigen]]s limits the response (i.e., when there are few [[pathogens]] present). In their study, Stefanova et al. (2002) injected an anti-[[MHC class II]] [[antibody]] into mice expressing a single type of MHC Class II molecule (H-2<sup>b</sup>) to temporarily prevent CD4+ T cell-MHC interaction. [[Drug-naïve|Naive]] [[CD4+ T cells]] (those that have not encountered non-self antigens before) recovered from these mice 36 hours post-anti-MHC administration showed decreased responsiveness to the [[antigen]] pigeon [[cytochrome c]] peptide, as determined by [[ZAP70]] [[phosphorylation]], proliferation, and [[interleukin 2]] production. Thus Stefanova et al. (2002) demonstrated that self-MHC recognition (which, if too strong may contribute to autoimmune disease) maintains the responsiveness of CD4+ T cells when foreign antigens are absent.<ref>{{cite journal | vauthors = Stefanová I, Dorfman JR, Germain RN | title = Self-recognition promotes the foreign antigen sensitivity of naive T lymphocytes | journal = Nature | volume = 420 | issue = 6914 | pages = 429–434 | date = November 2002 | pmid = 12459785 | doi = 10.1038/nature01146 | s2cid = 993284 | bibcode = 2002Natur.420..429S | url = https://zenodo.org/record/1233257 }}</ref>
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