|作者：||Li Guanggang, Wulan Hasi, Song Zongchang, Paik Paul A, Tsao Ming L, Goodman Gary M, MacEachern Paul T, Downey Robert S, Jankowska Anna J, Rabinowitz Yaron M, Learch Thomas B, Song David Z, Yuan Ji J, Zheng Shihang, Zheng Zhendong|
1Affiliated Bayi Brain Hospital, General Hospital of Beijing Military Command, Beijing, 100700, China.
2Department of Plastic and Reconstructive Surgery, PLA General Hospital, Beijing, 100853, China.
3Department of Oncology, The 155th Central Hospital of PLA, Kaifeng, 475003, China.
4Roswell Park Cancer Institute, Buffalo, NY, United States of America.
5Georgetown University Medical Center, Washington DC, United States of America.
6University of Maryland Medical Center. Baltimore, MD, United States of America.
7University Hospital, University of British Columbia, Vancouver, BC, Canada.
8University Hospital, University of British Columb
|刊名：||PloS one, 2015, Vol.10 (7), pp.e0134591|
|原始语种摘要：||Helicobacter pylori infection occurs in more than half of the world's population and is the main cause for gastric cancer. A series of lifestyle and nutritional factors, such as tobacco smoking and obesity, have been found to elevate the risk for cancer development. In this study, we sought to determine the immunological aspects during H. pylori infection and gastric cancer development. We found that B cells from H. pylori-infected patients presented altered composition and function compared to uninfected patients. IL-10-expressing CD24+CD38+ B cells were upregulated in H. pylori-infected patients, contained potent regulatory activity in inhibiting T cell pro-inflammatory cytokine secretion, and responded directly to H. pylori antigen stimulation. Interestingly, in H. pylori-infected... smoking subjects and obese subjects, the number of IL-10+ B cells and CD24+CD38+ B cells were reduced compared to H. pylori-infected asymptomatic subjects. Regulatory functions mediated by CD24+CD38+ B cells were also impaired. In addition, gastric cancer positive patients had reduced IL-10-producing B cell frequencies after H. pylori-stimulation. Altogether, these data suggest that in H. pylori-infection, CD24+CD38+ B cell is upregulated and plays a role in suppressing pro-inflammatory responses, possibly through IL-10 production, a feature that was not observed in smoking and obese patients.|