Salem Mohamed Labib, E El Naggar Randa, A El Naggar Sabry, A Mobasher Maysa, H Mahmoud Mohamed, Badr Gamal
Immunology and Biotechnology Unit, Department of Zoology, Faculty of Science, Tanta University, Tanta, Egypt AND Center of Excellence in Cancer Research, Tanta University, Tanta, Egypt.
Immunology and Biotechnology Unit, Department of Zoology, Faculty of Science, Tanta University, Tanta, Egypt.
Iran J Allergy Asthma Immunol. 2017 Dec;16(6):537-553.
The liver has unique microenvironment which is known to induce tolerance of cytolytic CD8+ T cells to hepatic and extra hepatic antigens, resulting in persistence of infection of the liver by the hepatitis B and C viruses. However, under some conditions, functional immune responses can be elicited in the liver in particular to show preferential retention of activated CD8+ T cells. It is not clear whether this retention depends on the type of the exogenous immunostimulatory or the endogenous innate immune cells. The T cell receptor (TCR) transgenic OT-1 (CD8+) mouse model was used in which OT-1 cells were harvested from the spleen of the donor and transferred into recipient mice followed by immunization with OVA peptide followed by injection of GM-CSF, CCL21 chemokine, or cytokines (IL-2, IL-12, or IL-15), or the toll-like receptor 3 agonist poly(I:C). Co-administration of any of these immunostimulatory agents relatively augmented the retention of CD8+ T cells with different levels of effects. Compared to spleen, the Ag-specific CD8+ T cells in the liver showed higher activities including expansion, proliferation, apoptosis and memory responses as well as cytolytic function. While depletion of natural killer cells significantly decreased the hepatic retention of the antigen-specific T cells, depletion of Kupffer cells showed opposite effect. Taken together, the antigen reactive T cells in the liver have higher activities than their counterparts in the peripheral tissues such as spleen. These data have important clinical implications for designing immunotherapeutic protocols toward the liver diseases.
肝脏具有独特的微环境,已知该微环境可诱导细胞溶解性CD8 + T细胞对肝脏和肝外抗原产生耐受性,从而导致乙型和丙型肝炎病毒在肝脏持续感染。然而,在某些条件下,肝脏中可引发功能性免疫反应,特别是表现出活化的CD8 + T细胞的优先滞留。目前尚不清楚这种滞留是否取决于外源性免疫刺激剂的类型或内源性固有免疫细胞。使用了T细胞受体(TCR)转基因OT-1(CD8 +)小鼠模型,其中从供体脾脏中收获OT-1细胞并转移到受体小鼠中,随后用OVA肽免疫,然后注射GM-CSF、CCL21趋化因子或细胞因子(IL-2、IL-12或IL-15),或Toll样受体3激动剂聚肌胞苷酸(poly(I:C))。共同施用这些免疫刺激剂中的任何一种相对增强了CD8 + T细胞的滞留,且效果水平不同。与脾脏相比,肝脏中抗原特异性CD8 + T细胞表现出更高的活性,包括扩增、增殖、凋亡和记忆反应以及细胞溶解功能。虽然自然杀伤细胞的耗竭显著降低了抗原特异性T细胞在肝脏中的滞留,但枯否细胞的耗竭则显示出相反的效果。综上所述,肝脏中的抗原反应性T细胞比外周组织如脾脏中的对应细胞具有更高的活性。这些数据对于设计针对肝脏疾病的免疫治疗方案具有重要的临床意义。