期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 198, 期 12, 页码 1887-1897出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20030621
关键词
MAP kinase signaling cascades; immunosuppression; host-pathogen interactions; calcium signaling
资金
- Telethon [E.1161] Funding Source: Medline
Helicobacter pylon toxin, VacA, damages the gastric epithelium by erosion and loosening of tight junctions. Here we report that VacA also interferes with T cell activation by two different mechanisms. Formation of anion-specific channels by VacA prevents calcium influx from the extracellular milieu. The transcription factor NF-AT thus fails to translocate to the nucleus and activate key cytokine genes. A second, channel-independent mechanism involves activation of intracellular signaling through the mitogen-activated protein kinases MKK3/6 and p38 and the Rac-specific nucleotide exchange factor, Vav. As a consequence of aberrant Rac activation, disordered actin polymerization is stimulated. The resulting defects in T cell activation may help H. pylori to prevent an effective immune response leading to chronic colonization of its gastric niche.
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