Following the inspiring opening speech, "Future Perspective of Cancer Immunotherapy," delivered by Nobel Prize and Tang Prize laureate Prof. Tasuku Honjo at the 14th Asia Pacific Federation of Pharmacologist Conference (APFP) on November 26, the 2020 Tang Prize Laureate's Lecture for Biopharmaceutical Science, co-organized by the Tang Prize Foundation and The Pharmacological Society in Taiwan, China, took place at the 14th APFP at 1:30 p.m. (GMT+8) on November 27. Co-hosted by Dr. Wen-Chang Chang, chair of Taipei Medical University's board of directors, and Dr. Yun Yen, chair professor at Taipei Medical University, this special session featured lectures delivered by three winners for the 2020 Tang Prize in Biopharmaceutical Science, Drs. Charles Dinarello, Marc Feldmann, and Tadamitsu Kishimoto, providing valuable informaiton on the role cytokines play in inflammation and the COVID-19 disease as well as possible treatments.
The first lecture by Dr. Dinarello, titled "Interleukin-1: The Prime Mediator of Systemic and Local Inflammation," began with his purification of leukocytic pryogen from human white blood cells in 1971. It then took him six years to identify two fever-producing molecules, later named IL-1αand IL-1β. In 1977, the research outcomes were published in the Proceedings of the National Academy of Sciences, and for Dr. Dinarello, "that was an important step in the history of cytokine biology," because many people in the field of life science were encouraged to study the immune system's influence on human physiology. As a result, cytokine biology expanded rapidly. He also talked about how after the early experiments in humans, "the history of cytokines being used as a treatment changed dramatically," and the focus was shifted to "inhibiting cytokines, such as IL-1, such as TNF, such as IL-6." To help the audience understand the complicated network constituted by the pro-inflammatory molecules of the IL-1 family, Dr. Dinarello elaborated on the signal transduction of IL-1 family members, their pro- and anti-inflammatory characteristics, and the symptoms of different inflammatory diseases, so as to ease the way for the audience to get a proper grasp of the second half of the lecture which centered on "the clinical application of Il-1 blockade." IL-1 overproduction, as Dr. Dinarello remarked, is a common cause of many diseases. IL-1Ra, on the other hand, can inhibit Il-1αandβ, and block the IL-1R signaling. Anakinra, a recombinant human IL-1Ra has been produced. It is used to treat rheumatoid arthritis and can also prevent glycemic disorders in type 2 diabetes. Moreover, canakinumab, an anti-IL-1βmonoclonal antibody successfully developed by Novartis, has been approved in a variety of diseases, ranging from rare hereditary diseases, rheumatic diseases, autoimmune and inflammatory diseases, to cardiovascular diseases. The most exciting news involving canakinumab is the clinical trial, CANTOS, which unexpectedly proved that canakinumab has an important role in treating cancer. Therefore, Dr. Dinarello believes that blocking IL-1 can usher in the dawn of a new cancer treatment.
The second speaker, Dr. Feldmann, shared his views on "Translating Molecular Insights in Autoimmunity into Effective Therapy." The emphasis of the first half of his lecture was on how he discovered that anti-TNF can be effective in treating rheumatoid arthritis. Administrating either high or low doses of this drug can block TNF while also rapidly reducing the production of other inflammatory mediators. In their earlier experiments, Dr. Feldmann and his team demonstrated that around 50% of people with rheumatoid arthritis responded to the combination therapy using anti-TNF and the cancer drug methotrexate. That led him to believe that "we've got a long way to go before every patient is cured." During the second half of the talk, Dr. Feldmann informed us that "TNF is a very unusual meditator, because it has two different targets: TNF receptor-1(TNFR1), which drives inflammation, and TNF receptor 2, which does the very opposite. So if you block all of TNF, you block of receptors. You block inflammation, but you also prevent the body's attempt to dampen down the inflammation." Therefore, h...
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