.
The basic finding of the study is that the tumors formed earlier and were more abundant in the absence of IL-13Ra1 than in its presence.
Mice were used as experimental animals in the study. Murine T cells show little expression of the IL-13 receptor and, somewhat surprisingly, the study found that IL-13 receptor deficiency led to an increase in the number of immune-suppressing regulatory T cells during the development of skin cancer.
While the exact mechanism remains unclear, it is clear that when the IL-13 receptor expression on the cell surface is absent during the development of cancer, the number of regulatory T cells increases, and the immune response is suppressed (skewed).
The study also shed new light on the relationship between inflammation and cancer. The abnormal accumulation of inflammatory cells after IL-13Ra1 deficiency strongly suggests that there is a chronic oxygen deficiency in the tumors associated with this abnormal new blood vessel formation. This potentially drives the formation of cancer.
This is an interesting finding because cellular signaling via the IL-13 receptor has been considered a very specific allergy-related phenomenon and it regulates the body’s immune defense (inflammatory response) against cancer.
Researchers will continue to investigate the current finding at the molecular level. The current findings are published in the Journal of Investigative Dermatology.
Two new lines of research opened up in the wake of this finding: both the basic immunological effect of immune response on cancer development and the molecule-level role of IL-13Ra1 in it, and on the other hand the effect of the IL-13 receptor on neovascularization.
Source: Medindia
