New study explores role of IL-4 in immunoregulation, psoriasis

IL-4, an abbreviation for the endogenous signaling molecule Interleukin 4, could play an important role in addressing psoriasis and strengthening the immune system, according to a new study at the Technische Universität München (TUM) and the University of Tübinge.

 

Scientists at both universities conducted studies on an animal model and on patients to explore IL-4’s mechanism of action to substantiate its ability to inhibit inflammation, which is already well known. Using a translational approach of applying laboratory findings to patients without delay, the scientists first used human and mouse cells to unravel the molecular effects of IL-4 on inflammation. They discovered that IL-4 inhibits specific immune cells in a natural way by preventing the cells from synthesizing and releasing two signaling molecules, IL-23 and IL-17.

 

Psoriasis and other autoimmune diseases such as multiple sclerosis and rheumatoid arthritis are associated with undue tissue damage resulting from poorly coordinated or misdirected immune reactions that can trigger inflammation even in the absence of external agents.

 

“Together with colleagues from Tübingen, we were able to show in earlier studies that the signaling molecule IL-4 is a promising candidate for the treatment of psoriasis,” said Prof. Tilo Biedermann, who holds the chair for Dermatology and Allergology and is director of the Clinic and Polyclinic for Dermatology and Allergology at TUM. 

 

“However, before IL-4 can be used as a standardized medication, we have to understand the exact mechanism of action—and we’ve now succeeded in doing just that. The discovery is very interesting in that IL-23 activates special T-cells in the body, thus triggering inflammation. Evidently IL-4 is able to effectively block this pathway,” added Professor Biedermann. 

 

The scientists also found out in subsequent experiments with mice that administration of IL-4 specifically inhibits inflammation of the skin via this mechanism. To verify the findings from the animal model in a patient study, the scientists gave subcutaneous injections of IL-4 to twenty-two patients with psoriasis over a period of six weeks. They examined samples from the patients’ affected skin areas before and after the treatment.

 

Experiment results confirmed the findings of the earlier study. IL-23 and IL-17, which were in high levels in the patients’ inflamed and itchy skin before treatment with IL-4, became barely detectable after treatment, indicating the disappearance of inflammation and psoriatic skin changes.

 

Professor Biedermann said their study results show that IL-4 very selectively and successfully suppresses inflammation. “This therapeutic approach could therefore be very interesting for the treatment of other autoimmune diseases. Moreover, we now have a better understanding of how IL-4 functions as an important ‘checkpoint’ in the immune system and will be able to better appreciate and exploit its significance in the future,” he noted.