Tregs in Allergies and Autoimmune Diseases

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Table of Contents

Abstract
Introduction
Goals of the Study
Techniques
Findings
Discussion
Conclusion
Works Cited

Abstract

Tregs refer to subpopulations of T cells that play a role in suppressing the autoimmunity of diseases. They maintain self-tolerance and homeostasis of body’s immunity. Tregs inhibit the proliferation of T cells; hence, they play a role in the prevention of the autoimmunity.

In a lipopolysaccharide challenge carried out using mice models, Tregs were found to control CD4⁺T cells from causing hypersensitivity, which pointed to their indispensable role in the control of autoimmunity diseases.

The investigation of the role of Tregs in allergies entailed in vitro experiments in which models of mouse CD4⁺CD25⁺ T cells were used. The cells were found to suppress differentiation of Th2 from CD4⁺ cells, which inhibited IgE. The IgE acts against antigens that cause allergies.

Introduction

Tregs (regulatory T cells) prevent autoimmune diseases and infections that arise from organ pathogens. The roles of Tregs in autoimmune diseases and allergies have resulted in a lot of interest. As a result, there have been many studies by clinical researchers to ascertain the functions of Tregs in the allergies and autoimmune diseases. For example, Okeke, Okwor and Uzonna (656) conducted a study to investigate the functions of Tregs.

The study entailed a lipopolysaccharide (LPS) in which Tregs were found to prevent unregulated immune activation. In relation to the allergies, the studies investigated the effects of subsets of Tregs in influencing IgE population. The following paper investigates Tregs and their roles in the prevention of allergies and autoimmune diseases.

Goals of the Study

Prevention of autoimmune diseases is one of the key areas of interest in studies related to Tregs. Schmidt, Oberle and Krammer (4) noted that the function of Tregs in the maintenance of peripheral tolerance cannot be underestimated. Therefore, the first goal of this study is to determine the function of Tregs in the immune activation. The second goal is to determine the role of Tregs in the regulation of allergic diseases.

Techniques

In the study to investigate the role of Tregs in the maintenance of peripheral tolerance, knock out models of murine lymphocyte gene were used. The study included the use of non-lethal dose of LPS. Mice that were SCID or RAG 1 deficient and lacked the T and B cells were investigated for the LPS susceptibility (Okeke, Okwor and Uzonna 656).

In the investigation of the role of Tregs in reducing allergic sensitization, studies that included in vitro differentiation of Th2 from CD4⁺T cells (Robinson, Larché & Durham 1389).

Findings

In the investigation of the role of Tregs in the autoimmunity, depletion of the Tregs resulted in increased sensitivity to LPS. However, the mice that lacked T and B cells were not sensitive to LPS. The depletion of Tregs resulted in increase in CD4 (+) T cells proliferation that responded to the LPS challenge. The CD4 (+) T cells are normally pathologic.

The cells exaggerated the activation of the immune system, which negatively affected the survival of LPS (Okeke, Okwor and Uzonna 659). Investigation of functions of Tregs in allergies found that models of mice CD4⁺CD25⁺T cells suppressed the differentiation of Th2 from CD4⁺T cells. The high levels of IgE were reduced by CD4⁺CD25^–T cells.

Transgenic mice with monoclonal populations of T cells increased the levels of IgE. In vitro experiments of models of mouse CD4⁺CD25⁺T cells suppressed the differentiation of Th2 in vitro from CD4⁺T cells. The monoclonal populations of T cells increased the levels of IgE.

Discussion

The subpopulations of T cells prevent infections induced organ pathology. Tregs act by inhibiting the TCR Induced proliferation. In the LPS challenge, the use of the murine suppressed the T cells proliferation thus Tregs produced TGF^–β that controls autoimmunity. According to Okeke, Okwor and Uzonna (661), subsets of Tregs both in mice and in humans play an importance role in the pathogenesis of autoimmune diseases.

Tregs control the homeostasis of T cells by suppressing the proliferation of effectors T cells. The result is the increase in self-tolerance. In vivo experiments have showed that the absence of Tregs leads to autoimmune diseases such as gastritis, arthritis, and thyroiditis.

IgE is produced in atopic allergic sensitization. The IgE protects the body from environmental antigens. In normal cases, the control of allergies is done by use of allergen injection immunotherapy (Robinson, Larché and Durham 1389). The mechanism involves the modulation of Th2 response.

According to Palomares (1236), the subsets of Tregs share common features of Foxp3 expression and inhibit the cytokine IL-10 (TGF^–β). The inhibition of functional Tregs compromises the body’s response to allergies. The implication is that the Tregs prevent the responses of IgE. Thus, Tregs contribute to the early development of allergies.

Conclusion

Tregs enhance self-tolerance and maintain homeostasis by suppression of effectors T cells. The inhibition of the proliferation of T cells results in actions that control autoimmunity diseases. On the other hand, the inhibitory properties of Tregs reduce the population of IgE; hence, compromising body’s response to allergies. Therefore, in designing therapies for allergies, the actions of Tregs and their effects on IgE should be considered.

Works Cited

Okeke, Emeka, Ifeoma Okwor, and Jude Uzonna. “Regulatory T cells restrain CD4+ T cells from causing unregulated immune activation and hypersensitivity to lipopolysaccharide challenge.” The Journal of Immunology 193.2 (2014): 655- 662. Print.

Palomares, Oscar. “Role of Tregs in immune regulation of allergic diseases.” European Journal of Immunology 40.5 (2010): 1232-1240. Print.

Robinson, Douglas, Mark Larché, and Stephen Durham. “Tregs and allergic disease.” Journal of Clinical Investigation 114.10 (2004): 1389-1391.Print.

Schmidt, Angelika, Nina Oberle, and Peter Krammer. “Molecular mechanisms of Treg- mediated T cell suppression.” Frontiers in Immuneology 3.1 (2012): 2-13. Print.

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