Tim-3 alters the balance of IL-12/IL-23 and drives TH 17 cells: Role in hepatitis B vaccine failure during hepatitis C infection

• Published in: Vaccine Vol. 31; no. 18; pp. 2238 - 2245
• Main Authors: Wang, Jia M, Ma, Cheng J, Li, Guang Y, Wu, Xiao Y, Thayer, Penny, Greer, Pamela, Smith, Ashley M, High, Kevin P, Moorman, Jonathan P, Yao, Zhi Q
• Format: Journal Article
• Language: English
• Published: 2013
• Subjects: Allergy and Immunology; hepatitis B virus; ALT; HS; IL-23; signal transducer and activator of transcription; interleukin-12; Tim-3; SD; alanine transaminase; hepatitis C virus; Hepatitis B vaccine; Hepatitis C infection; programmed death-1; HBV; peripheral blood mononuclear cells; AST; hepatitis B vaccine non-responder; KLRG-1; IL-12; PBMC; interleukin-23; interleukin-17; STAT; HBV-NR; hepatitis B vaccine responder; healthy subject; HBV-R; HIV; T cell immunoglobulin mucin domain-3; IL-17; human immunodeficiency virus; HCV; killer cell lectin-like receptor subfamily G member 1; aspartate transaminase; PD-1; standard deviation
• ISSN: 0264-410X
• DOI: 10.1016/j.vaccine.2013.03.003

Highlights • We explore the mechanisms underlying vaccine failure in hepatitis C-infected subjects. • Hepatitis B vaccine failure was associated with up-regulation of Tim-3 on monocytes. • Vaccine failure was associated with dysregulated IL-12/23 expressions in monocytes. • Vaccine failure was also associated with TH 17 cell accumulation. • Ex vivo Tim-3 blockade corrected the imbalance of IL-12/IL-23/TH 17.