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首页> 外文期刊>Infection and immunity >Major Histocompatibility Complex Class I Peptide Presentation after Salmonella enterica Serovar Typhimurium Infection Assessed via Stable Isotope Tagging of the B27-Presented Peptide Repertoire
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Major Histocompatibility Complex Class I Peptide Presentation after Salmonella enterica Serovar Typhimurium Infection Assessed via Stable Isotope Tagging of the B27-Presented Peptide Repertoire

机译：肠沙门氏菌血清鼠伤寒沙门氏菌感染后主要组织相容性复杂的I类肽呈递通过稳定的同位素标记B27呈现的肽库进行评估。

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Reactive arthritis (ReA) induced by infection with several gram-negative bacteria is strongly associated with expression of the major histocompatibility complex class I molecule HLA-B27. It is thought that due to the intracellular lifestyle of ReA-inducing bacteria, bacterial fragments can be presented by HLA-B27. Cytotoxic T cells recognizing such bacterial peptides or other induced host peptides could cross-react with self peptides presented in the joints, giving rise to disease. Studies to analyze the B27 peptide repertoire in relation to infection were severely hampered, as complex peptide profiles obtained from separate infected and noninfected cell preparations had to be compared. For this study, we applied a new approach to examine the effect of Salmonella enterica serovar Typhimurium infection on the B27 peptide repertoire presented by the HLA-B*2704 subtype associated with disease. Firstly, we showed that both host cell and S. enterica serovar Typhimurium proteins can be tagged metabolically with stable-isotope-labeled arginine. We then designed experiments so that either the tagged endogenous or tagged bacterial B*2704-presented peptide repertoires from infected cells could be analyzed by mass spectrometry from single peptide preparations that included uninfected controls. Using this new approach, we found no evidence for significant changes in endogenous B*2704 peptide presentation after infection or for any S. enterica serovar Typhimurium-derived B27-bound peptide. In conclusion, the hypothesis that S. enterica serovar Typhimurium induces changes in B27 peptide presentation could not be supported.
机译：由几种革兰氏阴性细菌感染引起的反应性关节炎（ReA）与主要组织相容性复合物I类分子HLA-B27的表达密切相关。据认为，由于ReA诱导细菌的细胞内生活方式，HLA-B27可以呈现细菌片段。识别这种细菌肽或其他诱导的宿主肽的细胞毒性T细胞可能与关节中存在的自身肽发生交叉反应，从而引起疾病。分析B27肽库与感染相关的研究受到严重阻碍，因为必须比较从单独的感染和未感染细胞制备物中获得的复杂肽谱。在这项研究中，我们采用了一种新方法来检查肠炎沙门氏菌血清鼠伤寒沙门氏菌感染对与疾病相关的HLA-B * 2704亚型呈现的B27肽库的影响。首先，我们显示了宿主细胞和 S。肠鼠血清型鼠伤寒蛋白可以用稳定同位素标记的精氨酸进行代谢标记。然后，我们设计了实验，以便可以通过质谱分析包括未感染对照的单肽制剂，分析来自感染细胞的标记内源性或标记细菌B * 2704呈递的肽库。使用这种新方法，我们没有发现感染后或任何 S内源性B * 2704肽呈递显着变化的证据。鼠伤寒鼠伤寒杆菌来源的B27结合肽。总而言之，假设是 S。肠伤寒鼠伤寒沙门氏菌诱导B27肽呈递的改变不能得到支持。

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