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Prevention of Type 1 Diabetes by Regulation of the Immune System

Commentary Open Access
Department of Biochemistry, SSR Medical College, Mauritius
*Corresponding authors: Robby Kumar
Department of Biochemistry
SSR Medical College, Mauritius
E-mail: kumarrobby@gmail.com
 
Received May 09, 2012; Published July 26, 2012
 
Citation: Kumar R (2012) Prevention of Type 1 Diabetes by Regulation of the Immune System. 1: 154. doi:10.4172/scientificreports.154
 
Copyright: © 2012 Kumar R. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 
Abstract
 
Immune mediated beta cell destruction is one of the major causes for type1 diabetes mellitus, which makes immune system a primary target for intervention for prevention of type1 diabetes. This review is done to know the immunological interventions for T1DM prevention viz immunosuppressive agents, Antigen Specific Immunotherapy, Anti-CD3 Antibodies and Anti CD20 antibodies.
 
Keywords
 
Diabetes mellitus; Immunosuppressive agents; Anti CD3 Antibodies
 
Introduction
 
Diabetes mellitus is a metabolic disorder characterized by hyperglycemia due to absolute and relative insulin deficiency. Type 1 diabetes mellitus also known as insulin dependent diabetes mellitus accounts for 5-10% of all causes of the syndrome, is a T-cell–mediated autoimmune disease that begins, in many cases, three to five years before the onset of clinical symptoms, continues after diagnosis, and can recur even after islet transplantation.1-3 Theeffector mechanisms which is responsible for the destruction of beta cells involves the action of cytotoxic T cells as well as soluble T-cell products [1,2].
 
Immunological Intervention for Treatment of Diabetes Mellitus Type 1 Immunosuppressive Agent
 
These are the agents which decreases the destruction of pancreatic beta cells. One of the example for the immunosuppressive agent is Cyclosporin A which blocks cytokine production by all T cells thus limiting production of the T-cell, it also prevents the secretion of cytokines, which is animportant direct mediators of beta cell destruction, these includes Interferon C (IFN-c) and Tumor Necrosis Factor a (TNF-a) [3,4]. Cyclosporine A, hasbeen reported to decrease destruction of beta cells [5]. Although Cyclosporin A targeted cytokine production, other broadspectrum immunosuppressive regimens also may be effective in preventingthe loss of insulin production [6]. These immunosuppressive agents are nephrotoxic and have other side effects making it highly inappropriate for long term uses [6].
 
Antigen Specific Immunothreapy
 
These strategies are based on the factthat a response to antigen is affected by many factors which include the antigenic signal strength, costimulation, and the cytokine environment. Therefore, by modulating these parameters, it is possible to divert pathogenic responses of the antigens into a protective, nonpathogenic response [4,6]. In addition to modifying the strength of the T-cell receptor signal with altered ligands or adjuvants, the prevention of antigen can be altered [7,8,9]. By this way type 1 Diabetes Mellitus can be prevented by inducing immune regulation to the administrated antigen.
 
Anti-Cd3 Antibodies
 
Anti CD 3 molecules contain FcR- binding portion which is responsible for T-Cell activation signals and other effects of T-Cells, thus by eliminating FcR binding portion of Anti CD3 molecule type 1 diabetes mellitus can be prevented. It has been reported that non- FcR binding antibody induces previously activated T-Cells but naïve cells were unaffected. Also, the other inhibitory effects were limited to the previously activated T-helper cells- which are involved and are present in pancreas of subjects with type1 diabetes mellitus. Anti CD 3 antibody molecule may induce tolerance to autoimmune destruction of pancreatic beta cells preventing diabetes mellitus type1. The non FcR binding antibodies activates signal to T cells resulting in release of Interleukin 10 (IL 10). The conventional Anti CD3 Antibodies release IFN-c [10-13].
 
An Anti-Cd20 Antibody
 
These molecules inhibits B cells, it has been reported that anti CD 20 Antibodies also provoke C-peptide responses. Through their action prevents type1 diabetes but long term action have not been studied in detail [4].
 
 
References