Age is an important determinant in humoral and T cell responses to immunization with hepatitis B surface antigen

2013 ◽  
Vol 9 (7) ◽  
pp. 1466-1476 ◽  
Author(s):  
Carina Rosenberg ◽  
Nicolai V. Bovin ◽  
Lone Valentin Bram ◽  
Eigil Flyvbjerg ◽  
Mogens Erlandsen ◽  
...  
Keyword(s):  
T Cell ◽  
Hepatitis B ◽  
Surface Antigen ◽  
Important Determinant ◽  
Hepatitis B Surface Antigen ◽  
T Cell Responses ◽  
Cell Responses

scholarly journals T cell responses to hepatitis B surface antigen are detectable in non-vaccinated individuals

2008 ◽  
Vol 14 (16) ◽  
pp. 2529 ◽  
Author(s):  
Martin R Weihrauch ◽  
Michael von Bergwelt-Baildon ◽  
Milos Kandic ◽  
Martin Weskott ◽  
Winfried Klamp ◽  
...  
Keyword(s):  
T Cell ◽  
Hepatitis B ◽  
Surface Antigen ◽  
Hepatitis B Surface Antigen ◽  
T Cell Responses ◽  
Cell Responses

Efficient priming of simian/human immunodeficiency virus (SHIV)-specific T-cell responses with DNA encoding hybrid SHIV/hepatitis B surface antigen particles

Vaccine ◽  
2004 ◽  
Vol 22 (27-28) ◽  
pp. 3535-3545 ◽  
Author(s):  
Anne-Laure Puaux ◽  
Delphine Marsac ◽  
Stéphane Prost ◽  
Mandal K Singh ◽  
Patricia Earl ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Hepatitis B ◽  
Surface Antigen ◽  
Hepatitis B Surface Antigen ◽  
T Cell Responses ◽  
Dna Encoding ◽  
Cell Responses ◽  
Immunodeficiency Virus

T-Cell Responses to Hepatitis B Surface Antigen in Lung Transplant Recipients

2007 ◽  
Vol 27 (9) ◽  
pp. 1248-1252 ◽  
Author(s):  
Mary S Hayney ◽  
Nicholas A Wiegert ◽  
Frances L Pelsue ◽  
Renee M Fohl ◽  
Ewa Jankowska-Gan ◽  
...  
Keyword(s):  
T Cell ◽  
Hepatitis B ◽  
Surface Antigen ◽  
Lung Transplant ◽  
Hepatitis B Surface Antigen ◽  
T Cell Responses ◽  
Transplant Recipients ◽  
Cell Responses ◽  
Lung Transplant Recipients

HBV-specific T cell responses in low replicating inactive carrier patients are independent of Hepatitis B surface antigen load

2018 ◽  
Vol 68 ◽  
pp. S793-S794
Author(s):  
U.S. Gill ◽  
N. Hansi ◽  
N.L. Bert ◽  
K. Kunasegaran ◽  
G.E. Dolman ◽  
...  
Keyword(s):  
T Cell ◽  
Hepatitis B ◽  
Surface Antigen ◽  
Hepatitis B Surface Antigen ◽  
T Cell Responses ◽  
Inactive Carrier ◽  
Cell Responses

scholarly journals Type I Interferon Signaling Prevents Hepatitis B Virus-Specific T Cell Responses by Reducing Antigen Expression

2018 ◽  
Vol 92 (23) ◽  
Author(s):  
Keigo Kawashima ◽  
Masanori Isogawa ◽  
Susumu Hamada-Tsutsumi ◽  
Ian Baudi ◽  
Satoru Saito ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
T Cell ◽  
Hepatitis B ◽  
Type I Interferon ◽  
T Cell Responses ◽  
Antigen Expression ◽  
Type I ◽  
Interferon Signaling ◽  
Cell Responses ◽  
B Virus

ABSTRACT Robust virus-specific CD8+ T cell responses are required for the clearance of hepatitis B virus (HBV). However, the factors that determine the magnitude of HBV-specific CD8+ T cell responses are poorly understood. To examine the impact of genetic variations of HBV on HBV-specific CD8+ T cell responses, we introduced three HBV clones (Aa_IND [Aa], C_JPN22 [C22], and D_IND60 [D60]) that express various amounts of HBV antigens into the livers of C57BL/6 (B6) (H-2b) mice and B10.D2 (H-2d) mice. In B6 mice, clone C22 barely induced HBV-specific CD8+ T cell responses and persisted the longest, while clone D60 elicited strong HBV-specific CD8+ T cell responses and was rapidly cleared. These differences between HBV clones largely diminished in H-2d mice. Interestingly, the magnitude of HBV-specific CD8+ T cell responses in B6 mice was associated with the HB core antigen expression level during the early phase of HBV transduction. Surprisingly, robust HBV-specific CD8+ T cell responses to clone C22 were induced in interferon-α/β receptor-deficient (IFN-αβR–/–) (H-2b) mice. The induction of HBV-specific CD8+ T cell responses to C22 in IFN-αβR–/– mice reflects enhanced HBV antigen expression because the suppression of antigen expression by HBV-specific small interfering RNA (siRNA) attenuated HBV-specific T cell responses in IFN-αβR–/– mice and prolonged HBV expression. Collectively, these results suggest that HBV genetic variation and type I interferon signaling determine the magnitude of HBV-specific CD8+ T cell responses by regulating the initial antigen expression levels. IMPORTANCE Hepatitis B virus (HBV) causes acute and chronic infection, and approximately 240 million people are chronically infected with HBV worldwide. It is generally believed that virus-specific CD8+ T cell responses are required for the clearance of HBV. However, the relative contributions of genetic variation and innate immune responses to the induction of HBV-specific CD8+ T cell responses are not fully understood. In this study, we discovered that different clearance rates between HBV clones after hydrodynamic transduction were associated with the magnitude of HBV-specific CD8+ T cell responses and initial HB core antigen expression. Surprisingly, type I interferon signaling negatively regulated HBV-specific CD8+ T cell responses by reducing early HBV antigen expression. These results show that the magnitude of the HBV-specific CD8+ T cell response is regulated primarily by the initial antigen expression level.

scholarly journals Up-regulation of a death receptor renders antiviral T cells susceptible to NK cell–mediated deletion

2012 ◽  
Vol 210 (1) ◽  
pp. 99-114 ◽  
Author(s):  
Dimitra Peppa ◽  
Upkar S. Gill ◽  
Gary Reynolds ◽  
Nicholas J.W. Easom ◽  
Laura J. Pallett ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Hepatitis B ◽  
Nk Cells ◽  
Human Liver ◽  
Large Population ◽  
Death Receptor ◽  
T Cell Responses ◽  
Dependent Manner ◽  
Cell Responses

Antiviral T cell responses in hepatotropic viral infections such as hepatitis B virus (HBV) are profoundly diminished and prone to apoptotic deletion. In this study, we investigate whether the large population of activated NK cells in the human liver contributes to this process. We show that in vitro removal of NK cells augments circulating CD8+ T cell responses directed against HBV, but not against well-controlled viruses, in patients with chronic hepatitis B (CHB). We find that NK cells can rapidly eliminate HBV-specific T cells in a contact-dependent manner. CD8+ T cells in the liver microcirculation are visualized making intimate contact with NK cells, which are the main intrahepatic lymphocytes expressing TNF-related apoptosis-inducing ligand (TRAIL) in CHB. High-level expression of the TRAIL death receptor TRAIL-R2 is found to be a hallmark of T cells exposed to the milieu of the HBV-infected liver in patients with active disease. Up-regulation of TRAIL-R2 renders T cells susceptible to caspase-8–mediated apoptosis, from which they can be partially rescued by blockade of this death receptor pathway. Our findings demonstrate that NK cells can negatively regulate antiviral immunity in chronic HBV infection and illustrate a novel mechanism of T cell tolerance in the human liver.

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