如果嗜睡症是一種選擇性的自身免疫性腦疾病 它會引發其他疾病的可能性仍然被發現 事實上 丘腦病變可產生臨床上很容易識別的表型 嗜睡 猝倒症 可能發現有可能使這些 很可能其他自身免疫性疾病的大腦區域選擇性

引起下丘腦分泌的細胞損失是激烈的研究課題 嗜睡症是緊密相關的人類白細胞抗原 HLA DQB1基因* 0602 米格諾特等 2001 暗示一種自身免疫性調解 儘管 20年的調查 但是 從來沒有明確的證據被發現 最近 全基因組關聯研究 shingles symptoms GWAS 已完成其中發現一個遺傳協會 shingles symptoms Rs1154155 在T細胞受體α TCRα 升ocus 在多民族 亞洲人 高加索人 黑人 Hallmayer等 2009 由於 T細胞受體 是 受體的HLA肽 介紹 這一結果表明自身免疫反應 有意思的是 另一項研究最近發現的患病率增加鏈球菌感染標記物在發生案件猝睡症 阿蘭等人 2009 由於眾所周知的鏈球菌感染引發的其他自體免疫的表現 如錫德納姆的舞蹈病和風濕性心髒病發作性睡病也可能是鏈球菌感染後自身免疫性疾病
有趣的是 猝睡症發作是沒有關聯的檢測炎症 我們建議 在猝睡症 免疫介導素細胞破壞是有選擇性和自限性 無明顯抗原傳播的 有限的抗原表位傳播可能是一個功能的神經元作為一種免疫保護的目標 並能解釋在檢測自身免疫異常困難 事實上 人類白細胞抗原II類神經元的表達仍然不斷壓抑 不像在膠質細胞 甚至在面對局部炎症 可能是重要的 shingles symptoms 特異性這一過程可能也解釋了遺傳協會電阻溫度係數 協會沒有發現在其他自身免疫性疾病 在此模型中 Rs1154155或緊密連鎖標記區域內的TCRJα 法沃爾發生了非常具體的南軍TCRα致病性T細胞克隆重組或標記的編碼段的J內改變 改變TCRα肽具有約束力
如果嗜睡症是一種選擇性的自身免疫性腦疾病 它會引發其他疾病的可能性仍然被發現 事實上 丘腦病變可產生臨床上很容易識別的表型 嗜睡 猝倒症 可能發現有可能使這些 很可能其他自身免疫性疾病的大腦區域選擇性 選擇性神經細胞損失 不發生 但較少有具體的臨床療效 如精神病表現 最近發現 人類白細胞抗原易感基因是精神分裂症和狂躁抑鬱症的大規模 GWAS研究提供一些支持這一概念 斯特凡松等人 2009 我們希望 在時間 猝睡症不僅告知我們有關的睡眠 但對其他自身免疫性疾病的大腦
 
Narcolepsy affects 1 in 2,000 people. It is characterized by excessive daytime sleepiness, cataplexy and abnormal transitions from wakefulness to REM sleep. Recent findings have shown that the disorder is caused by the loss of ∼70,000 hypothalamic neurons (Peyron et al., 2000). These neurons produce an excitatory neuropeptide called hypocretin/orexin. The lack of this peptide results in narcolepsy, in both humans and animals. The hypocretin system is now the object of pharmaceutical efforts in the area of sleep and sleep disorders.
The cause of the hypocretin cell loss is the subject of intense research. Narcolepsy is tightly associated with human leukocyte shingles symptoms antigen (HLA) DQB1*0602 (Mignot et al., 2001), shingles symptoms suggesting an autoimmune mediation. Despite decades of investigations, however, no definitive evidence has ever been found. Recently, a genome wide association study (GWAS) was completed which found a genetic association with Rs1154155 within shingles symptoms the T-cell receptor alpha (TCRα) l ocus across multiple ethnic groups (Asians, Caucasians, African American) (Hallmayer et al., 2009). Since the TCR is the receptor for HLA-peptide presentation, this result suggests shingles symptoms autoimmunity. Interestingly, another study recently found an increased prevalence of streptococcal infection markers in onset cases of narcolepsy (Aran et al., 2009). As streptococcal infections are known to trigger other autoimmune manifestations, e.g., Sydenham's chorea and rheumatic heart disease, narcolepsy may also be a post-streptococcal autoimmune condition.
Interestingly, narcolepsy onset is not associated with detectable inflammation. We suggest that in narcolepsy, the immune-mediated destruction of hypocretin cells is selective and self-limited, without significant epitope-spreading. Limited epitope spreading may be a feature of neurons as an immune-protected target, and could explain difficulties in detecting autoimmune abnormalities. The fact that HLA class II expression in neurons remains constantly repressed (unlike in glial cells), even in the face of local inflammation, may be important. The specificity of this process may also explain shingles symptoms the genetic association shingles symptoms with TCRs, an association not found in other autoimmune diseases. In this model, Rs1154155 or a tightly linked marker within the TCR Jα region, fa-vors the occurrence of a very specific V-J TCRα pathogenic T-cell clone recombinants or marks a coding change within a J segment that alters TCRα-peptide binding.
If narcolepsy is a selective autoimmune brain disease, it raises shingles symptoms the possibility that other diseases remain to be discovered. The fact that hypocretin lesions can produce a clinically very easily identifiable phenotype (narcolepsy-cataplexy) may have made these discoveries possible. It is likely that other brain area selective autoimmune diseases (with selective neuronal cell loss) do occur but have less specific clinical effects, shingles symptoms such as psychiatric manifestations. The recent finding that HLA is a susceptibility locus for schizophrenia shingles symptoms and bipolar disorder in large scale GWAS studies provide some support for this concept (Stefansson et al., 2009). We hope that in time, narcolepsy will not only inform us about sleep, but about other autoimmune diseases of the brain. shingles symptoms References Aran, A., Lin, L., Nevsimalova, S., Plazzi, G., Hong, S. C., Weiner, K., Zeitser, J., and Mignot, E. (2009). Elevated anti-streptococcal antibodies in patients with recent narcolepsy onset. Sleep 32, 979-983. Hallmayer, J., Faraco, J., Lin, L., Hesselson, shingles symptoms S., Winkelmann, J., Kawashima, M., Mayer, G., Plazzi, G., Nevsimalova, S., Bourgin, P., et al. (2009). Narcolepsy is strongly associated with the T-cell receptor alpha locus. Nat. Genet. 41, 708-711. Mignot, E., Lin, L., Rogers, W., Honda, Y., Qiu, X., Lin, X., Okun, M., Hohjoh, H., Miki, T., Hsu, S. H, et al. (2001). Complex HLA-DR and -DQ interactions confer risk of narcolepsy-cataplexy in three ethnic groups. Am. J. Hum. Genet. 68, 686-699. Peyron, C., Faraco, shingles symptoms J., Rogers, W., Ripley, B., Ove