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标题: AASLD2019[690]乙型肝炎病毒中抗原表达的调控 临床用药物类别 [打印本页]

作者: StephenW    时间: 2019-11-1 19:00     标题: AASLD2019[690]乙型肝炎病毒中抗原表达的调控 临床用药物类别

690
MODULATING ANTIGEN PRESENTATION IN HEPATITIS B VIRUS
INFECTED HEPATOCYTES WITH DRUG CLASSES IN CLINICAL
DEVELOPMENT IMPACTS CD8 T CELL RECOGNITION
Adrian Kuipery, University Health Network; Immunology,
University of Toronto; Toronto Center for Liver Disease,
Toronto General Hospital Research Institute, Harry L. A.
Janssen, Toronto Centre for Liver Disease, Francis Family
Liver Clinic, Toronto General Hospital and Adam J. Gehring,
Toronto Centre for Liver Disease, Toronto General Hospital
Research Institute, University Health Network
Background: Hepatitis B virus (HBV) specific CD8 T cell
immunity is essential for the control of HBV infection. Short
interfering RNA (siRNA) and immunomodulatory drugs in
clinical development for chronic Hepatitis B (CHB) have the
potential to modulate antigen expression and hepatocyte
antigen presentation The impact of these treatments on CD8
T recognition of infected hepatocytes remains to be clarified.
We hypothesize that siRNA and immunomodulatory drugs
alter presentation of HBV antigens, impacting CD8 T cell
recognition Methods: HepG2-NTCP cells were infected with
HBV and treated with siRNA targeting all HBV transcripts, or
exposed to conditioned media harvested after 24h treatment of
PBMC with the TLR-8 agonist, TL:506. Infected HepG2-NTCP
cells were then co-cultured with HBV-specific CD8 T cells
recognizing immunodominant epitopes C18-27 and S183-
191 to measure antigen presentation Results: Treatment
of HBV infected HepG2-NTCP cells with HBV-specific siRNA
inhibited HBV replication and suppressed HBV antigen
production Reduced antigen production suppressed CD8 T
cell recognition by 80% as early as 2 days post treatment
CD8 T cell recognition began to recover by 8 days post siRNA
treatment but was still suppressed by 48 1%, consistent with
the slow recovery of antigen expression in infected HepG2-
NTCP To investigate effects of immunomodulation, we
stimulated PBMCs with TL8:506. TL8:506 stimulation strongly
induced proinflammatory cytokines, including IFN-γ, IL-1β,
IFN-λ, and TNF-α. When infected HepG2-NTCP were cultured
with conditioned media, CD8 T cell recognition of both the
S183-191 and C18-27 epitopes was enhanced, resulting in a
15 and 3 fold increase in the proportion of IFN-y positive CD8
T cells, respectively Conclusion: Therapies in development
for the treatment of CHB alter CD8 T cell recognition of HBV
infected cells A deeper understanding of the effects of new
drugs on interactions between hepatocytes and CD8 T cells
may help optimize combination therapies.
作者: StephenW    时间: 2019-11-1 19:00

690
乙型肝炎病毒中抗原表达的调控
临床用药物类别感染的肝细胞
发展影响CD8 T细胞的识别
Adrian Kuipery,大学健康网;免疫学
多伦多大学多伦多肝病中心
多伦多总医院研究所,Harry L. A.
Janssen,多伦多弗朗西斯家族肝病中心
多伦多总医院肝脏诊所和Adam J. Gehring,
多伦多总医院多伦多肝病中心
大学卫生网络研究所
背景:乙型肝炎病毒(HBV)特异性CD8 T细胞
免疫力对于控制HBV感染至关重要。短
干扰RNA(siRNA)和免疫调节药物
慢性乙型肝炎(CHB)的临床发展有
调节抗原表达和肝细胞的潜力
抗原呈递这些治疗对CD8的影响
T识别感染的肝细胞仍有待澄清。
我们假设siRNA和免疫调节药物
改变HBV抗原的呈递,影响CD8 T细胞
识别方法:用HepG2-NTCP细胞感染
HBV,并用靶向所有HBV转录本的siRNA进行治疗,或
暴露于24h处理后收获的条件培养基中
具有TLR-8激动剂的PBMC,TL:506。感染的HepG2-NTCP
然后将细胞与HBV特异性CD8 T细胞共培养
识别免疫优势表位C18-27和S183-
191测量抗原呈递结果:治疗
HBV特异性siRNA检测被HBV感染的HepG2-NTCP细胞
抑制HBV复制并抑制HBV抗原
产生减少的抗原产生抑制了CD8 T
最早在治疗后2天就能识别80%的细胞
siRNA后8天CD8 T细胞识别开始恢复
治疗,但仍被抑制48 1%,与
感染的HepG2中抗原表达的缓慢恢复
NTCP为了研究免疫调节的作用,我们
TL8:506刺激的PBMC。 TL8:506强烈刺激
诱导的促炎细胞因子,包括IFN-γ,IL-1β,
IFN-λ和TNF-α。当感染HepG2-NTCP时进行培养
在条件培养基中,CD8 T细胞对两种
S183-191和C18-27表位得到增强,导致
IFN-γ阳性CD8的比例分别增加15和3倍
结论:疗法正在发展中
用于治疗CHB改变对HBV的CD8 T细胞识别
被感染的细胞对新的作用有更深的了解
药物对肝细胞和CD8 T细胞相互作用的影响
可能有助于优化组合疗法。




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