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Tsai, Tsung-Yu; Huang, Ming-Ting; Sung, Pei-Shan; Peng, Cheng-Yuan; Tao, Mi-Hua; Yang, Hwai-I; Chang, Wei-Chiao; Yang, An-Suei; Yu, Chung-Ming; Lin, Ya-Ping; Bau, Ching-Yu; Huang, Chih-Jen; Pan, Mei-Hung; Wu, Chung-Yi; Hsiao, Chwan-Deng; Yeh, Yi-Hung; Duan, Shiteng; Paulson, James C; Hsieh, Shie-Liang
The Journal of clinical investigation, 6/2021, Letnik: 131, Številka: 11Journal Article
Chronic hepatitis B (CHB) infection is rarely eradicated by current antiviral nucleos(t)ide analogues. We found that alpha2,6-biantennary sialoglycans of HBV surface antigen (HBsAg) bound human SIGLEC-3 (CD33) by IP and ELISA, and the binding affinity between SIGLEC-3 and alpha2,6-biantennary sialoglycans was determined by biolayer interferometry (equilibrium dissociation constant KD: 1.95 * 10.sup.-10 + or - 0.21 * 10.sup.-10 M). Moreover, HBV activated SIGLEC-3 on myeloid cells and induced immunosuppression by stimulating immunoreceptor tyrosine-based inhibitory motif phosphorylation and SHP-1/-2 recruitment via alpha2,6-biantennary sialoglycans on HBsAg. An antagonistic anti-SIGLEC-3 mAb reversed this effect and enhanced cytokine production in response to TLR-7 agonist GS-9620 in PBMCs from CHB patients. Moreover, anti-SIGLEC-3 mAb alone was able to upregulate the expression of molecules involved in antigen presentation, such as CD80, CD86, CD40, MHC-I, MHC-II, and PD-L1 in CD14.sup.+ cells. Furthermore, SIGLEC-3 SNP rs12459419 C, which expressed a higher amount of SIGLEC-3, was associated with increased risk of hepatocellular carcinoma (HCC) in CHB patients (HR: 1.256, 95% CI: 1.027-1.535, P = 0.0266). Thus, blockade of SIGLEC-3 is a promising strategy to reactivate host immunity to HBV and lower the incidence of HCC in the CHB patient population.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
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Vir: Osebne bibliografije
in: SICRIS
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