D'Elios Mario M, Czinn Steven J
Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
Helicobacter. 2014 Sep;19 Suppl 1:19-26. doi: 10.1111/hel.12156.
Helicobacter pylori colonizes mucosa, activates Toll-like and Nod-like receptors, and usually elicits a gastric T-helper 1/17 (Th1/Th17) type of immune response. Among several bacterial factors, the secreted peptidyl prolyl cis, trans-isomerase of H. pylori represents a key factor driving Th17 inflammation. A complex and fascinating balance between H. pylori and host factors takes part in the gastric niche and is responsible for the chronicity of the infection. Novel insights into the innate and adaptive responses against H. pylori, dealing with gastric epithelial cells, cytokines, and immune evasion have been elucidated over the past year and are discussed for the development of an effective vaccine.
幽门螺杆菌定殖于黏膜,激活Toll样受体和Nod样受体,通常引发胃辅助性T细胞1/17(Th1/Th17)型免疫反应。在多种细菌因素中,幽门螺杆菌分泌的肽基脯氨酰顺反异构酶是驱动Th17炎症的关键因素。幽门螺杆菌与宿主因素之间复杂而迷人的平衡参与胃生态位的形成,并导致感染的慢性化。过去一年里,针对幽门螺杆菌的固有免疫和适应性免疫反应,涉及胃上皮细胞、细胞因子和免疫逃逸方面的新见解已得到阐明,并就开发有效疫苗进行了讨论。