Pathogenic role of heat shock proteins gammadelta-T cells in inflammatory skin diseases

慢性和潜伏性感染病灶常常引起或触发身体远处的致病过程，用“局灶性感染”一词来解释。免疫遗传学上保守的蛋白，热休克蛋白（HSPs），在暴露于高温或其他环境后在细胞中被诱导。这一现象已被研究与宿主对细菌的防御和自身免疫的诱导有关，因为细菌热休克蛋白具有免疫原性，是免疫监测的目标，而感染应激后诱导的哺乳动物热休克蛋白能够被相同的免疫机制识别。我们开始研究各种炎症性皮肤病中分枝杆菌HSP65抗体的产生，以便将这种所谓的“局灶性感染”联系起来。1992年，我们获得了大约200名患有各种皮肤病的患者的数据。与正常组比较，掌足底脓疱病（PPP）、牛皮癣（Pso）、荨麻疹和带状疱疹患者Ig . More抗体在ELISA板上检测麻风分枝杆菌HSP65。类过敏性紫癜患者的抗体水平未升高。1993年，我们进一步研究了HSP65抗体与细菌感染引发的皮肤炎性疾病的相关性。新收集的PPP患者分为以慢性扁桃体炎或牙周炎为感染病灶的和不以慢性扁桃体炎为感染病灶的两组。该ELISA技术在492 nm处的OD值显示PPP与感染灶的差异有统计学意义（p<0.01） （n=7,0.230(] SY.+-),[）0.065，平均值（]SY.+-）。没有它(SD)和购买力平价(n = 12, 0.139 (SY。+ - 0.066。())。在银屑病中，收集的患者根据银屑病病变类型分为三组：急性管状银屑病（PGA），这是一种特殊类型的银屑病，通常由steptococcus感染引起，斑块型银屑病（PV）和脓疱型银屑病（PP）。PGA的抗hsp65igg水平为0.174(]SY.+-. [)0.032 (n=4)， PV为0.101(]SY.+-. [)0.053 (n=12)， PP为0.087(]SY.+-. [)0.025 (n=6)， PGA与其他组之间差异有统计学意义（p=0.0165, PGA - PV; p=0.001, PGA - PP）。抗hsp65igg的升高与细菌感染引起的银屑病和皮肤白化炎症有关。少

Chronic and latent infectious focus often causes or triggers the pathogenic process in distant part(s) of the body, being explained by a term "focal infection". Immunogenetically well-conserved proteins, heat shock proteins (HSPs), are inducied in cells after exposure to elevated temperature or others. This phenomenon has been investigated in relation to both host-defense to dacteria and induction of autoimmunity, since bacterial HSPs are immunogenic and targetted by immune surveilance, while mammalian HSPs induced after infectious stress are able to be recognized by the same immune mechanism. We started to investigate antibody production to mycobacterial HSP65 in various inflammatory skin diseases in order to correlate this so-called 'focal infection".In 1992, we obtained data from approximately 200 patients with various skin diseases. In comparison to normal group, patients with palmoplantar pustulosis (PPP), psoriasis (Pso), urticaria, and herpes zoster frequently showed elevated Ig … More G antibody to HSP65 from Mycobacterium leprae assayd on ELISA plates. In patients with anaphylactoid purpura the antibody level was not raised.In 1993, we further investigated correlation between antibody to HSP65 and skin inflammatory diseases triggered by bacterial infection. Patients with PPP were newly collected and divided into groups with and without chronic tonsilitis or periodontitis as infectious focus. OD at 492 nm in this ELISA technique revealed significant (p<0.01) difference between PPP with infectious focus (n=7,0.230(〕SY.+-.〔)0.065, mean(〕SY.+-.〔)SD) and PPP without it (n=12,0.139(〕SY.+-.〔)0.066). IN psoriasis, collected patients were divided into three groups according to types of psoriatic lesions : acute guttate psoriasis (PGA) that is a particular type of psoriasis induced often after steptococcal infection, plaque-type psoriasis (PV) and psutular-form psoasis (PP). The anti-HSP65IgG levels were 0.174(〕SY.+-.〔)0.032 for PGA (n=4), 0.101(〕SY.+-.〔)0.053 for PV (n=12) and 0.087(〕SY.+-.〔)0.025 for PP (n=6), showing significant changes between PGA and others (p=0.0165, PGA - PV ; p=0.001, PGA - PP).Elevation of anti-HSP65IgG was found in relation to bacterial infection-induced psoriatic and leukotactic inflammation in the skin. Less