Bittner-Eddy P D, Fischer L A, Costalonga M
Division of Periodontology, Department of Developmental and Surgical Sciences, School of Dentistry, University of Minnesota, Minneapolis, MN, USA.
Mol Oral Microbiol. 2013 Dec;28(6):452-66. doi: 10.1111/omi.12038. Epub 2013 Aug 14.
Chronic periodontitis is associated with Porphyromonas gingivalis infection. Although virulence factors of P. gingivalis are hypothesized to contribute to the pathogenesis of periodontitis, it is unclear whether the local CD4(+) T-cell-mediated response they elicit prevents or contributes to periodontal bone destruction. We hypothesize that major histocompatibility complex class II I-A(b) -binding peptides existing in Kgp and RgpA are presented to CD4(+) T cells during P. gingivalis oral colonization. The protein sequences of gingipains RgpA and Kgp, and OMP40 and OMP41 of P. gingivalis were scanned using an I-A(b) -binding matrix. From this analysis we identified 53 candidate peptides that had the potential to engage the peptide-binding groove of the I-A(b) molecule of C57BL/6 mice. An ELISpot-based screen revealed those peptide-primed effector/memory CD4(+) T cells that could be re-stimulated in vitro with P. gingivalis or the peptide itself to produce interleukin-17A or interferon-γ. Two immunodominant peptides, Kgp467-477 (pKgp) and RgpA1054-1064 /Kgp1074-1084 (pR/Kgp) were identified and engineered to be displayed on I-A(b) molecular tetramers. Peptide pR/Kgp is conserved across all sequenced P. gingivalis strains. C57BL/6 mice were orally inoculated with P. gingivalis strain 53977 and cervical lymph node cells were stained with phycoerythrin-conjugated pKgp::I-A(b) and pR/Kgp::I-A(b) tetramers. We found that only pR/Kgp::I-A(b) bound with the desired specificity to gingipain-specific CD4(+) T cells. The pR/Kgp::I-A(b) tetramer complex will allow the identification of effector/memory CD4(+) T cells specific for two virulence factors of P. gingivalis strains associated with periodontal disease.
慢性牙周炎与牙龈卟啉单胞菌感染有关。尽管推测牙龈卟啉单胞菌的毒力因子会导致牙周炎的发病机制,但尚不清楚它们引发的局部CD4(+) T细胞介导的反应是预防还是促进牙周骨破坏。我们推测,在牙龈卟啉单胞菌口腔定植过程中,存在于Kgp和RgpA中的主要组织相容性复合体II类I-A(b)结合肽会呈递给CD4(+) T细胞。使用I-A(b)结合矩阵扫描牙龈蛋白酶RgpA和Kgp以及牙龈卟啉单胞菌的OMP40和OMP41的蛋白质序列。通过该分析,我们鉴定出53种候选肽,它们有可能与C57BL/6小鼠I-A(b)分子的肽结合槽结合。基于ELISpot的筛选揭示了那些肽引发的效应/记忆CD4(+) T细胞,这些细胞在体外可以被牙龈卟啉单胞菌或肽本身重新刺激以产生白细胞介素-17A或干扰素-γ。鉴定出两种免疫显性肽,Kgp467-477(pKgp)和RgpA1054-1064 /Kgp1074-1084(pR/Kgp),并设计使其展示在I-A(b)分子四聚体上。肽pR/Kgp在所有测序的牙龈卟啉单胞菌菌株中都是保守的。用牙龈卟啉单胞菌菌株53977口服接种C57BL/6小鼠,并用藻红蛋白偶联的pKgp::I-A(b)和pR/Kgp::I-A(b)四聚体对颈淋巴结细胞进行染色。我们发现只有pR/Kgp::I-A(b)以所需的特异性与牙龈蛋白酶特异性CD4(+) T细胞结合。pR/Kgp::I-A(b)四聚体复合物将允许鉴定与牙周疾病相关的牙龈卟啉单胞菌菌株的两种毒力因子特异性的效应/记忆CD4(+) T细胞。