Thymosin α1 and Its Role in Viral Infectious Diseases: The Mechanism and Clinical Application
Article reviews Thymosin α1 (Tα1) and its role in viral infectious diseases, particularly focusing on its mechanism and clinical application. Tα1 is an immunostimulatory peptide that enhances immune responses in viral infections like COVID-19, hepatitis B, hepatitis C, and AIDS by interacting with Toll-like receptors and activating various signal pathways.
Thymosin α1 (Tα1) is an immunostimulatory peptide that plays a crucial role in enhancing immune responses in viral infectious diseases such as hepatitis B, hepatitis C, and AIDS. It is produced by thymic stromal cells and is involved in T cell differentiation, development, and maturation. Tα1 can interact with Toll-like receptors such as TLR3/4/9, TLR2, and TLR7, activating downstream signal pathways like IRF3, NF-κB, p38MAPK, and MyD88. This activation leads to the proliferation and activation of immune cells like T cells, B cells, macrophages, and natural killer cells, thereby enhancing both innate and adaptive immune responses.
Tα1 has high immunomodulatory and immune-enhancing properties being utilized in various clinical applications. The peptide is highly conserved, expressed in multiple mammalian organs, and has been found to have 10-1000 times higher activity than other thymosin fractions. Its clinical efficacy in treating viral infections is well-documented, but a systematic review analyzing its exact impact on immune function in these diseases is lacking, making it an area of interest for further research.
Thymosin α1 can affect various viral infectious diseases, including hepatitis B, hepatitis C, and acquired immune deficiency syndrome (AIDS). Additionally, Tα1 has been studied for its potential therapeutic applications in treating COVID-19. Furthermore, Tα1 has been shown to modulate immune responses and exert effects on immune cells such as T cells, B cells, macrophages, and natural killer cells.
Tα1 influences the immune response stages to COVID-19 infection by potentially impacting the progression of the disease through its immunomodulatory effects. One study mentioned in the article highlights that the immune response to COVID-19 can be separated into three stages: stage I – asymptomatic incubation phase, stage II – non-severe symptomatic phase, and stage III – severe respiratory symptomatic stage. It is mentioned that during the third stage, patients may experience a cytokine storm response, where inflammatory markers like IL-6, IL-8, and TNF-α rise, leading to a hyperactive immune response.
Additionally, in vitro studies have indicated that Tα1 treatment can help alleviate lymphopenia in COVID-19 patients, promote the proliferation and differentiation of effector T cells, and regulate immune homoeostasis and cytokine storm in vivo. Furthermore, Tα1 has been found to dramatically reduce mortality within 28 days of critical illness by increasing the oxygenation index. For patients with severe lymphopenia whose CD8+ T cells or CD4+ T cells are below certain levels, Tα1 has been effective in increasing the number of T cells in the blood.
Overall, Tα1’s immunomodulatory properties may play a role in regulating the immune response stages by potentially mitigating the inflammatory response and aiding in the immune system’s ability to combat the infection at different stages of COVID-19 progression. Further research is needed to fully understand the impact of Tα1 on the immune response stages in COVID-19 patients and to optimize its therapeutic use in this context.
Full text can be found here: https://doi.org/10.3390/molecules28083539