Ko Eun Byeol, Kim Sun Kyung, Seo Ho Seong, Yun Cheol-Heui, Han Seung Hyun
Department of Oral Microbiology and Immunology, DRI, and BK21 Plus Program, School of Dentistry, Seoul National UniversitySeoul, South Korea.
Biotechnology Research Division, Korea Atomic Energy Research InstituteJeongeup, South Korea.
Front Microbiol. 2017 Mar 31;8:523. doi: 10.3389/fmicb.2017.00523. eCollection 2017.
Dendritic cells (DCs) play a pivotal role in the induction of immunity by recognition, capture, process, and presentation of antigens from infectious microbes. is able to cause life-threatening systemic diseases such as infective endocarditis. Serine-rich repeat (SRR) glycoproteins of are sialic acid-binding adhesins mediating the bacterial adherence to the host and the development of infective endocarditis. Thus, the SRR adhesins are potentially involved in the bacterial adherence to DCs and the maturation and activation of DCs required for the induction of immunity to . Here, we investigated the phenotypic and functional changes of human monocyte-derived DCs treated with wild-type or the SRR adhesin-deficient mutant. The mutant poorly bound to DCs and only weakly increased the expression of CD83, CD86, MHC class II, and PD-L1 on DCs compared with the wild-type. In addition, the mutant induced lower levels of TNF-α, IL-6, and IL-12 than the wild-type in DCs. When DCs sensitized with the mutant were co-cultured with autologous T cells, they induced weaker proliferation and activation of T cells than DCs stimulated with the wild-type. Blockade of SRR adhesin with 3'-sialyllactose markedly reduced binding and internalization, causing attenuation of the bacterial immunostimulatory potency in DC maturation. Collectively, our results suggest that SRR adhesins of are important for maturation and activation of DCs.
树突状细胞（DCs）在通过识别、捕获、处理和呈递来自感染性微生物的抗原诱导免疫方面发挥着关键作用。 能够引发危及生命的全身性疾病，如感染性心内膜炎。 的富含丝氨酸重复序列（SRR）糖蛋白是唾液酸结合黏附素，介导细菌对宿主的黏附以及感染性心内膜炎的发展。因此，SRR黏附素可能参与细菌对DCs的黏附以及诱导针对 的免疫所需的DCs的成熟和激活。在此，我们研究了用野生型 或SRR黏附素缺陷型突变体处理的人单核细胞衍生DCs的表型和功能变化。与野生型相比，突变体与DCs的结合较差，并且仅微弱增加DCs上CD83、CD86、MHC II类和PD-L1的表达。此外，突变体在DCs中诱导的TNF-α、IL-6和IL-12水平低于野生型。当用突变体致敏的DCs与自体T细胞共培养时，它们诱导的T细胞增殖和激活比用野生型刺激的DCs弱。用3'-唾液乳糖阻断SRR黏附素可显著降低 结合和内化，导致DC成熟中细菌免疫刺激效力减弱。总体而言，我们的结果表明 的SRR黏附素对DCs的成熟和激活很重要。
