Thymosin alpha 1 (T α 1) is a peptide, or small protein, produced naturally by the thymus gland. The thymus is where immune cells known as T cells mature and are released when prompted to do so by the T α 1 peptide. T cell production and action within the body is vital to adaptive immunity. This is the mode by which immune cells are able to recognize and kill foreign invaders. Specifically, T α 1 has been shown to enhance the function of certain immune cells called T and dendritic cells. These white blood cells play pivotal roles in the body’s defense process to anyone with a depressed immune system or suffering from an infection. Thymosin alpha 1 has three hallmark actions. It can improve immune modulation, it can be immune stimulating, or it can be immune dampening. It takes advantage of our innate and acquired immune system and does what is necessary depending on what is needed.
Benefits of Thymosin alpha 1:
- Enhances the function of certain immune cells called T and dendritic cells
- Effective for acute and chronic infections
- Help eradicate the unhealthy or senescent cells and stops the infection or cancer growth
- Exhibits antibacterial, antiviral and antifungal properties
- Suppresses tumor growth
- Increases vaccine effectiveness
- Protects against oxidative damage
T cells, for example, come in two forms: killer and helper T cells. Killer T cells are responsible for hunting down and destroying our body’s own cells that are cancerous or infected with bacteria or viruses. Helper cells work with the other cells of the immune system to orchestrate and carry out appropriate immune responses.
It is approved in more than 37 countries for the treatment of hepatitis B, hepatitis C, and as an adjunct to chemotherapy and various vaccines. T α 1 has been found to have a profound effect on the immune system and is the active ingredient in the immune modulating drug, Zadaxin®. Zadaxin® is used to treat hepatitis B and C and has been studied extensively for its ability to support an immune system that has been suppressed by chemotherapy in cancer patients. Additional possible indications are malignant melanoma, hepatocellular carcinoma, drug-resistant tuberculosis, chronic fatigue and Di George's syndrome as well as any chronic cancer or viral disease.
In addition to its use in the treatment of Hepatitis, AIDS, and cancer, T α 1 has shown great promise in the treatment of Lyme disease. This is unsurprising when one considers the large role the immune system plays in combating the disease.
T α 1 assists the immune system in the location and eradication of the Lyme bacteria and infected cells, while helping to prevent oxidative damage, thereby decreasing inflammation and enabling a better quality of life throughout treatment.
Thymosin alpha 1 is also a natural senolytic ( induce death of aging/senescent cells) that our thymus makes. It decreases with age because of thymic atrophy and this problem affects the production of thymosin alpha 1.
Thymosin alpha 1 can help bring back natural killer cell function and influence production of interleukin 1 beta, tumor necrosis factor, interleukin 6 and nuclear factor kappa B. It is also a senolytic because it helps senescent cells become more recognizable by macrophages and other cells in the immune system. Thymosin alpha 1 can activate and modulate the immune system to become a natural senolytic because in reality it's natural to the system. This is how Thymosin Alpha 1 acts as a senomodulator.
Studies have shown that individuals fighting infection have a lower amount of circulating T α 1 and suppressed helper T cell numbers compared to healthy individuals. This is problematic, as the optimal immune function is vital to recovery from infection. Supplementation with T α 1 has the potential for great therapeutic benefit for patients looking to strengthen their immune system and those suffering from an infection or autoimmune disease.
Immune Modulation with Thymosin Alpha 1 Treatment.pdf
Pica, F., Chimenti, M. S., Gaziano, R., Buè, C., Casalinuovo, I. A., Triggianese, P., … Garaci, E. (2016). Serum thymosin α 1 levels in patients with chronic inflammatory autoimmune diseases. Clinical & Experimental Immunology, 186(1), 39–45
Bozza, S., Gaziano, R., Bonifzi, P., et al. (2007). Thymosin alpha 1 activates the TLR9/MyD88/IRF7-dependent murine cytomegalovirus sensing for induction of anti-viral responses in vivo. International Immunology, 19, 1261–1270.
Chan, H. L., Tang, J. L., & Sung, J. Y. (2001). Thymosin a1 for the treatment of chronic hepatitis B virus (HBV) infection: A meta-analysis. In Paper presented at the digestive disease week 2001; May 20–23, Atlanta, GA.
Chen, J. (2007). Effects of thymosin α1 on cell immunity function in patients with septic shock. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue, 19, 153–155
Knutsen, A. P., Freeman, J. J., Mueller, K. R., Roodman, S. T., & Bouhasin, J. D. (1999).Thymosin-alpha1 stimulates maturation of CD34+ stem cells into CD3+4+ cells in an in vitro thymic epithelia organ coculture model. International Journal of Immunopharmacology, 21(1), 15–26.
Li, C., Wang, C.-H., Meng, Q.-H., Ye, S.-L., Wang, X.-J., & Jiang, C. (2007). Effect of the thymosin alpha 1 on immune function in aged chronic obstructive pulmonary disease during acute period. Chinese Journal of Hospital Pharmacy, 27(5), 637–639.
Romani, L., Bistoni, F., Gaziano, R., et al. (2004). Thymosin alpha 1 activates dendritic cells for antifungal Th1 resistance through toll-like receptor signaling. Blood, 103(11), 4232–4239.
Serafino, A., Pica, F., Andreola, F., Gaziano, R., Moroni, N., Moroni, G., et al. (2014). Thymosin α1 activates complement receptor-mediated phagocytosis in human monocytederived macrophages. Journal of Innate Immunity, 6(1), 72–88.
Serafino, A., Pierimarchi, P., Pica, F., et al. (2012). Thymosin alpha 1 as a stimulatory agent of innate cell-mediated immune response. Annals of the New York Academy of Sciences, 1269–1270, 43–50.
Serrate, S., Schulof, R., Leondaridis, L., Goldstein, A. L., & Sztein, M. B. (1987). Modulation of human natural killer cell cytotoxic activity, lymphokine production, and interleukin 2 receptor expression by thymic hormones. Journal of Immunology, 139, 2338–2343.