Haque Rizwanul, Chaudhary Archana, Sadaf Nadra
Centre for Biological Science (Biotechnology Programme), Central University of South Bihar, BIT Campus, Patna-800014. India
Endocr Metab Immune Disord Drug Targets. 2017;17(3):176-181. doi: 10.2174/1871530317666170818114454.
Chronic Arsenic (As) exposure continued to be a cause of major problem associated with different kind of diseases including skin problem and different types of cancer. As exposure leads to numerous other pathological conditions that affect millions of people worldwide on a regular basis. It was recently established that As toxicity affects immune system and modulates the function and survival of cells involved in immune regulation. Arsenic trioxide (As2O3) was reported to be an effective apoptosis inducer in a variety of cell types. Despite intensive research, the exact immune-modulatory role of As is poorly understood till now.
We reviewed the immunological imbalance caused due to As exposure and focused on regulatory T cells (Tregs cells). In this review, we mainly focused on role of As and its potential mechanisms in the induction and modulation of Tregs cells.
The multiple effects of As on immune system tend to decrease the immune surveillance system and increase the rate of infection, autoimmune disease, cancer and other immune mediated problems. As exposed individuals showed induction of oxidative stress, inflammation and impaired lymphocytes activation. The effect of As on T cell population is mainly attributed to altered expression of key immune regulator molecules impaired T cell functions, cytokines production, induction of apoptosis, and oxidative stress induction in T cells.
长期接触砷(As)仍然是导致包括皮肤问题和各类癌症在内的多种疾病的主要原因。砷暴露会引发许多其他病理状况,定期影响着全球数百万人。最近证实,砷毒性会影响免疫系统,并调节参与免疫调节的细胞的功能和存活。据报道,三氧化二砷(As2O3)在多种细胞类型中是一种有效的凋亡诱导剂。尽管进行了深入研究,但迄今为止,砷确切的免疫调节作用仍知之甚少。
我们回顾了因砷暴露导致的免疫失衡,并重点关注调节性T细胞(Tregs细胞)。在本综述中,我们主要关注砷在诱导和调节Tregs细胞中的作用及其潜在机制。
砷对免疫系统的多种作用往往会降低免疫监视系统,并增加感染、自身免疫性疾病、癌症和其他免疫介导问题的发生率。砷暴露个体表现出氧化应激、炎症和淋巴细胞活化受损。砷对T细胞群体的影响主要归因于关键免疫调节分子表达的改变、T细胞功能受损、细胞因子产生、凋亡诱导以及T细胞中的氧化应激诱导。