Authors: Yuri Fukui Kazushige Uchida Yutaku Sakaguchi Toshiro Fukui Akiyoshi Nishio Nobuaki Shikata Noriko Sakaida Yoshiko Uemura Sohei Satoi Kazuichi Okazaki
Publish Date: 2014/07/09
Volume: 50, Issue: 4, Pages: 435-444
Abstract
High serum immunoglobulin G4 IgG4 levels and IgG4positive plasma cell infiltration are characteristic of type 1 autoimmune pancreatitis AIP It is unclear whether innate immunity is a cause of type 1 AIP the possible involvement of microbial infection has been suggested in its pathogenesis To clarify the pathogenesis of type 1 AIP we investigated Tolllike receptors TLRs in type 1 AIP patientsWe studied nine cases of type 1 AIP with ten cases of alcoholic chronic pancreatitis ACP and three of the samples from nontumorous lesion of neuroendocrine tumor NET as control subjects We counted the number of TLR111positive cells immunohistochemically stained with antiTLR111 antibodies To identify TLRpositive cells in pancreata from type 1 AIP patients we used a doubleimmunofluorescence method and counted the numbers of identifiable CD68 CD163 CD123 and CD20positive cellsIn type 1 AIP TLR7 8815 ± 1755 TLR8 3852 ± 1489 and TLR10 3852 ± 0921 were highly expressed Only the ratio of TLR7 per monocyte was significantly higher in type 1 AIP 0053 ± 0012 than in ACP 0007 ± 0004 p 001 and nontumorous lesion of NET 0000 ± 0000 p 001 In type 1 AIP the CD163 to TLR7 ratio 0789 ± 0031 was significantly higher both than that of CD123 to TLR7 ratio 0034 ± 0006 p 0001 and CD20 to TLR7 ratio 0029 ± 0010 p 0001This study was partially supported by 1 GrantinAid for Scientific Research C of the Ministry of Culture and Science of Japan 26461038 23591017 24591020 2 GrantinAid for “Research for Intractable Diseases” Program from the Ministry of Labor and Welfare of Japan 3 GrantsinAid from CREST Japan Science and Technology Agency and 4 NEXTSupported Program for Strategic Research Foundation at Private Universities The authors thank Professor AHon Kwon for surgery of pancreas
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