Title:Immunomodulatory Role of Arsenic in Regulatory T Cells
VOLUME: 17 ISSUE: 3
Author(s):Rizwanul Haque*, Archana Chaudhary and Nadra Sadaf
Affiliation:Centre for Biological Science (Biotechnology Programme), Central University of South Bihar, BIT Campus, Patna-800014, Centre for Biological Science (Biotechnology Programme), Central University of South Bihar, BIT Campus, Patna- 800014, Centre for Biological Science (Biotechnology Programme), Central University of South Bihar, BIT Campus, Patna- 800014
Keywords:Arsenic (As), arsenic trioxide (As2O3), forkhead box P3 (FoxP3), regulatory T cells (Tregs cells), immuno-toxicity,
Immunomodulatory.
Abstract:Background and Objective: 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.
Methods: 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.
Conclusion: 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.
