Lessons Learned from the Differential Upregulation of 2?5?-Oligoadenylate Synthetase Genes in Systemic Sclerosis

Gabriel Magno De Freitas Almeida

doi:10.4172/1745-7580.s2.005

Abstract

Precise regulation of the immune system is crucial for homeostasis maintenance. Autoimmunities are complex disorders that have in common alterations in immune homeostasis, and in order to be fully understood approaches that take into consideration their complexity are needed. In systemic sclerosis patients, levels of type I Interferons and 2’5’-oligoadenylate synthetase genes are found upregulated. In 2013, an approach that quantified each individual 2’5’-OAS gene in patients revealed that there is a differential upregulation of this gene family. The hypothesis is that during the disease patient cells are refractory to circulating type I Interferons and that an unknown stimuli is differentially inducing OAS2 and OASL genes. It can be taken as an example that the complexity of the immune system and its components must be taken into consideration to satisfactory understand autoimmunities.

Highlights

The immune system is composed of biological agents and processes with the protection against infectious diseases being its most wellknown function
Autoimmunities are a group of complex disorders that have in common alterations of the immune homeostasis
Of the immune molecules found deregulated in Systemic Sclerosis, two important classes are type I Interferons and 2’5’-OAS genes [5,6]

Summary

Introduction

The immune system is composed of biological agents and processes with the protection against infectious diseases being its most wellknown function. Autoimmunities are a group of complex disorders that have in common alterations of the immune homeostasis. Even though it is hard to determine if these alterations are causes or consequences of the disorders, investigating the immune homeostasis disruption is crucial for better understanding these diseases [2].

Results

Conclusion