期刊
JOURNAL OF GASTROENTEROLOGY
卷 53, 期 3, 页码 449-460出版社
SPRINGER JAPAN KK
DOI: 10.1007/s00535-017-1390-6
关键词
Autoimmune pancreatitis; Basophil; TLR; M2 macrophage
资金
- Ministry of Culture and Science of Japan [17K09468, 15K09052]
- Research Program on Intractable Diseases from Ministry of Labor and Welfare of Japan
- Ministry of Education, Culture, Sports, Science and Technology of Japan from CREST Japan Science and Technology Agency
- Grants-in-Aid for Scientific Research [15K09053, 15K09052, 17K09468] Funding Source: KAKEN
Pathophysiology of type 1 autoimmune pancreatitis (AIP) is still unclear. We previously reported that M2 macrophages might play an important role in type 1 AIP. Recently, it has been reported that basophils regulate differentiation to M2 macrophages. In this study, we investigated basophils from the pancreatic tissue and peripheral blood of individuals with type 1 AIP. By using immunohistochemistry, we investigated basophils in pancreatic tissue from 13 patients with type 1 AIP and examined expression of toll-like receptors (TLRs) by these cells. Additionally, we obtained peripheral blood samples from 27 healthy subjects, 40 patients with type 1 AIP, 8 patients with alcoholic chronic pancreatitis, 10 patients with bronchial asthma, and 10 patients with atopic dermatitis, and analyzed activation of basophils by stimulating them with ligands of TLR1-9. We also compared TLR expression in basophils from the tissue and blood samples. Basophils were detected in pancreatic tissues from 10 of 13 patients with type 1 AIP. Flow cytometric analysis revealed that the ratios of basophils activated by TLR4 stimulation in type 1 AIP (9.875 +/- 1.148%) and atopic dermatitis (11.768 +/- 1.899%) were significantly higher than those in healthy subjects (5.051 +/- 0.730%; P < 0.05). Levels of basophils activated by TLR2 stimulation were higher in seven type 1 AIP cases. Furthermore, stimulation of TLR2 and/or TLR4, which were expressed by basophils in pancreas, activated basophils in peripheral blood. Basophils activated via TLR signaling may play an important role in the pathophysiology of type 1 AIP.
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