05). CD107a has relationship with viral load and HBeAg status.In vitro blockade NKP46, spontaneous cytolytic activity of NK cells against K562 cell lines and HepG2, HepG2.215 cell lines was decreased(p<0.05). Conlusion: NKP46 as a major activitory receptor has an obvious effect on the cytolytic function of
NK cells.NKP46 may be involved in both the suppression of HBV replication and HBV-associated liver damage underpinning the role of NK cells in the immunopathogenesis of chronic HBV infection. NKP46 was decreased significantly in high alanine aminotrans-ferases,high viral load and HBeAg positive group(a.b.c.d)The groups were divided by ALT,AST,HBV DNA and HBeAg status. Disclosures: The following people have nothing to disclose: Selleck RG7204 Wanyu
Li, Yanfang Jiang, Yanjun Cai, Yue Qi, Jinglan Jin, Xiaomei Wang, Junqi Niu To clarify the role of soluble CD40 (sCD40) in chronic hepatitis B (CHB), we measured the levels of sCD40 in sera from 132 CHB patients and 33 healthy individuals, and analyzed its association with serum levels of alanine transaminase (ALT) and aspartate transaminase (AST), and liver histological characteristics. The results indicated that sCD40 concentrations in CHB patients were significantly higher than in healthy controls (82.8 pg/ml vs 32.8 pg/ml). The sCD40 level was related to serum levels of ALT (r=0.487, p<0.001) and AST (r=0.492, p<0.001), and the intrahepatic Ishak necroinflammatory score (r=0.506, p<0.001) and fibrosis score 上海皓元 (r=0.395, p<0.001). MG-132 mouse CHB patients were distributed into four groups based on their Ishak necroinflammatory grading scores: minimal inflammation (scores 1-4), mild inflammation (score 5-8), moderate inflammation (score 9-12), and marked inflammation (score 13-18), which the mean of
sCD40 concentration was 61.8 pg/ml, 91.7 pg/ml, 139.0 pg/ml and 203.2 pg/ml respectively. The sCD40 concentration in CHB patients with minimal inflammation was significantly lower than that in patients with mild, moderate, and marked inflammation (p<0.01), and sCD40 concentration in CHB patients with mild inflammation was significantly lower than that in patients with moderate and marked inflammation (p<0.05). CHB patients with different fibrosis staging scores were distributed into four groups: normal (score 0), portal fibrotic expansion (score1 -2), bridging fibrosis (score3-4) and cirrhosis (score 5-6), which the mean of sCD40 concentration was 59.0 pg/ml, 66.1 pg/ml, 96.2 pg/ml and 157.2 pg/ml respectively. The difference in sCD40 levels between CHB patients without fibrosis (normal group) and healthy controls was not significant (p>0.05), whereas other groups showed significantly higher sCD40 concentrations than did healthy controls (p<0.001). sCD40 concentration in CHB patients with portal fibrotic expansion was significantly lower than that in patients with bridging fibrosis or cirrhosis (p<0.