Journal
JOURNAL OF IMMUNOLOGY
Volume 194, Issue 12, Pages 5644-5653Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1401942
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Grants-in-Aid for Scientific Research [26293383, 26670185, 15H04862, 26670575, 15H01365, 25293091, 15K15659] Funding Source: KAKEN
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Although Th1 and Th2 cells are known to be involved in allergic inflammatory diseases, the molecular mechanisms underlying their differentiation are incompletely understood. In this study, we identified CD155 as a costimulatory molecule on CD4(+) T cells. Importantly, CD155-mediated signaling induced Th1 development in both humans and mice, as evidenced by production of IFN-gamma and upregulation of Tbx21 transcription; these effects were independent of IL-12 but dependent on NF-kappa B-induced autocrine IFN-gamma that triggered positive feedback via STAT1 activation. Mice genetically deficient in CD155 or treated with anti-CD155 Ab exhibited attenuated Th1-type contact hypersensitivity. Thus, CD155 plays an important regulatory role in helper T cell differentiation and allergic diseases.
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