Interleukin 35
Interleukin 35 (IL-35) is a protein that in humans is encoded by the EBI3 and IL12A genes. It is a member of the interleukin family, a group of cytokines that are important in the immune system. IL-35 is a relatively newly discovered interleukin and is unique in that it is the only known interleukin to be produced by regulatory T cells (Tregs).
Structure[edit | edit source]
IL-35 is a heterodimeric cytokine composed of two subunits, EBI3 and IL12A. The EBI3 subunit is shared with Interleukin 27 (IL-27), while the IL12A subunit is shared with Interleukin 12 (IL-12). This sharing of subunits is a common feature among the interleukins and contributes to their functional diversity.
Function[edit | edit source]
IL-35 plays a crucial role in the immune system, particularly in the regulation of immune responses. It is produced by Tregs and acts to suppress the immune response, preventing excessive or unnecessary immune activity. This makes IL-35 important in the prevention of autoimmune diseases, where the immune system mistakenly attacks the body's own cells.
In addition to its role in immune regulation, IL-35 has also been found to promote the growth and differentiation of B cells, another type of immune cell. This suggests that IL-35 may have a broader role in the immune system than initially thought.
Clinical significance[edit | edit source]
Due to its role in immune regulation, IL-35 has been implicated in a number of diseases. High levels of IL-35 have been found in patients with cancer, where it is thought to suppress the immune response against the tumor. Conversely, low levels of IL-35 have been associated with autoimmune diseases such as rheumatoid arthritis and multiple sclerosis.
Research is ongoing into the potential use of IL-35 as a therapeutic target in these diseases. For example, increasing the levels of IL-35 in autoimmune diseases may help to suppress the overactive immune response, while decreasing IL-35 levels in cancer may help to boost the immune response against the tumor.
See also[edit | edit source]
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