The Th17/Treg axis: a key to understanding and treating autoimmune disorders

TL;DR

This paper explores how balancing Th17 and Treg cells can help treat autoimmune rheumatic diseases by reducing inflammation and improving treatment outcomes.

Contribution

The paper highlights the Th17/Treg balance as a novel key mechanism in autoimmune rheumatic diseases and its potential for therapeutic modulation.

Findings

Th17 and Treg cell imbalance is a key pathogenic mechanism in autoimmune rheumatic diseases.

The percentages of Th17 and Treg cells correlate with disease severity and treatment response.

Modulating the Th17/Treg balance offers a potential therapeutic strategy for autoimmune rheumatic diseases.

Abstract

In autoimmune rheumatic diseases (ARDs), T cells mistakenly attack the body’s own joints, skin, blood vessels, and other tissues, leading to chronic inflammation and tissue damage. Among these, the immune balance between T helper 17 lymphocytes (Th17) and regulatory T lymphocytes (Treg) is a foundation for maintaining normal immune function in the human body. An immune imbalance between Th17 and Treg cells is one of the key pathogenic mechanisms in ARDs. The percentages of Th17 and Treg cells can serve as important indicators for the severity of autoimmune diseases and treatment response. Therefore, by studying the origin and function of Th17 and Treg cells as well as the cytokine microenvironment that regulates their differentiation, we aim to modulate the immune state by restoring cellular balance. This approach is particularly relevant in ARDs such as rheumatoid arthritis, Sjögren’s syndrome, systemic lupus erythematosus, scleroderma, and ankylosing spondylitis. It also summarizes the current clinical application of disease-modifying anti-rheumatic drugs in regulating the balance between Th17 and Treg cells, with the aim of providing guidance for clinical practice.

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