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T helper 17 (Th17) and regulatory T (Treg) cell populations represent two distinct lineages of CD4+ T cells that maintain a critical balance in the immune system, often referred to as the Th17/Treg axis [1]. Th17 cells are pro-inflammatory, characterized by the expression of the transcription factor RORγt and the production of cytokines such as IL-17A and IL-22, which are vital for mucosal defense but also drive autoimmune pathology [2][3]. In contrast, Treg cells express the transcription factor Foxp3 and function to suppress immune responses and maintain self-tolerance [4]. An imbalance in this axis, typically favoring Th17 cells, is a hallmark of various autoimmune and inflammatory diseases, including psoriasis, rheumatoid arthritis, and multiple sclerosis [5]. Therapeutic strategies aim to restore this equilibrium by either inhibiting Th17-related pathways using monoclonal antibodies and small molecules or by enhancing Treg numbers and suppressive capacity [6]. [1] Noack, M., & Miossec, P. (2014). Autoimmunity Reviews. [2] Ivanov, I. I., et al. (2006). Cell. [3] Korn, T., et al. (2009). Annual Review of Immunology. [4] Sakaguchi, S., et al. (2008). Cell. [5] Lee, Y. K., et al. (2011). Immunity. [6] Bluestone, J. A., & Tang, Q. (2018). Nature Reviews Drug Discovery.
Modulation of the Th17/Treg balance through cytokine neutralization, transcription factor inhibition, or regulatory cell expansion.
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