Autoimmunity is that the system of immune responses of an organism against its own healthy cells and tissues. Any disease that results from such an aberrant immune reaction is termed an "autoimmune disease". Prominent examples include disorder , post-infectious IBS, DM type 1, Henloch Scholein Pupura (HSP) sarcoidosis, systemic LE (SLE), Sjögren syndrome, eosinophilic granulomatosis with polyangiitis, Hashimoto's thyroiditis, Graves' disease , idiopathic idiopathic thrombocytopenic purpura , Addison's disease , atrophic arthritis (RA), Marie-Strumpell disease , polymyositis (PM), dermatomyositis (DM) and MS (MS). Autoimmune diseases are fairly often treated with steroids. While a high level of autoimmunity is unhealthy, a coffee level of autoimmunity may very well be beneficial. Taking the experience of a beneficial think about autoimmunity further, one might hypothesize with intent to prove that autoimmunity is usually a self-defense mechanism of the mammal system to survive. The system doesn't randomly lose the power to differentiate between self and non-self, the attack on cells could also be the consequence of cycling metabolic processes necessary to stay the blood chemistry in homeostasis. Second, autoimmunity may have a task in allowing a rapid immune reaction within the early stages of an infection when the supply of foreign antigens 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 one sort of MHC Class II molecule (H-2b) to temporarily prevent CD4+ T cell-MHC interaction. Naive CD4+ T cells (those that haven't encountered any antigens before) recovered from these mice 36 hours post-anti-MHC administration showed decreased responsiveness to the antigen pigeon cytochrome 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.