1. What is Interleukin
Interleukin is a kind of cytokines, which plays a critical role in immunological regulation and homeostasis. It is originally discovered from leukocytes. Currently, it is found to be produced by a lot of cells including macrophages, lymphocytic cells with a solid structure and function.
2. Interleukin Family and Interleukin Receptor
The members of interleukin are wealthy which are named IL-1~IL-38.
The interleukin receptors can be classified as type I, type II and other type. The type II interleukin receptors include interleukin-10, 20, 22, 28 receptors, the other types include interleukin-1,8 receptors, the rest of them are type I interleukin receptors.
3. Common Signaling Pathway
4. Interleukin Function
Interleukin is important for transmitting information, activating and regulating immune cells, mediates the activation, proliferation and differentiation of T cells and B cells.
Interleukin-1 contains IL-1α and IL-1β. While the former is produced by diverse cells, the later is produced by some specific tissues. IL-1β is cleaved by caspase-1 which is formed by proteins termed as “the inflammasome”. It can lead to pain and short-time sleep, so that they study the relationship between fatigue and IL-1. IL-1 also can simulate the nitric oxides, chemokines, cytokines and ahesion molecules that destroy the cartilage, while the IL-1 receptor antagonist can inhibit the destruction of IL-1 through the completion of the same receptor. The study helps us to understand the pathology of these diseases.
Interleukin-2 is popular object in the past 36 years as it is important for the immunotherapy of many diseases including cancers. But the adverse of taking it is fearful.Thus, timing of IL-2 administration and different T cells status are crucial to IL-2 therapies.
Interleukin-10 is an anti-inflammatory cytokine. In the meanwhile, IL-10 suppresses the immune responses by modulating the T cells and antigen-presenting cells. By controlling the receptor of IL-10, we can resolve the chronic viral infection. The research was published in The Journal of Experimental Medicine in 2006.
Interleukin-18 is a regulator of cancer and autoimmune diseases. As a member of IL-1 family, it plays essential roles in inflammation process. It can cooperate with IL-12 to activate cytotoxic T cells (CTLs) and natural killer (NK) cells to produce IFNγ which may contribute to tumor immune. In addition, it can work with IL-23 to induce the secretion of IL-17. It has pros and cons effects in the treatment of many diseases.
5. Interleukin and Inflammation
Inflammation is a productive conduct to stimuli such as pathogens and damage cells. Its characters are heating, redness, swelling, pain and loss of function, sometimes accompanied with fever. Inflammasome activation leads to activation of caspase-1, resulting in the induction of apoptosis and the secretion of pro-inflammatory cytokines including IL-1β and IL-18. Without inflammation, we can not prevent harm from stimuli, but it can lead to chronic infection such as rheumatoid arthritis. Inflammation plays a key role in chronic inflammatory systemic diseases (CISD). There are overlaps between different CISD.
a. Interleukin-17 and Psoriasis
Psoriasis is a common, infammatory and chronic disease with the character of erythematous, scaly plaques. It is related to cardiovascular disease (CVD) such as artherosclerosis. As a result of immune dysregulation, its pathology refers to infammatory cytokines like tumor necrosis factor (TNF), interferon (IFN) and IL-1β, IL-6, IL-12, IL-17, IL-22, IL-23 produced from dendritic cells, T-helper cells and keratinocytes. Patients with psoriasis have more Th17 cells and higher level of IL-17A mRNA and protein. The recent study demonstrates over-expressing IL-17 causing increased inflammatory cells and levels of nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nitric oxide (NO) makes more severe psoriasis, and endothelial dysfunction. In contrast, blocking of IL-7 or the genes acting downstream of IL7 improve the severity of psoriasis.
b. Interleukin and Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a severe autoimmune disease accompanied with cartilage degradation, joint destruction and poor prognosis. The study indicates that the polymorphism of inflammation genes leads to the susceptibility of RA. Caspase-1 is a critical factor of RA, we can observe the reduction of RA in the caspase-1-/- mice model. Another member is NLRP1 which is related to the secretion of IL-1β and IL-18. Inhibiting the NLRP1 can ameliorate the symptom of RA.
c. Interleukin and Systemic Lupus Erythematosus
Systemic lupus erythematosus (SLE), accompanied with inflammatory joints, nephritis, mouth ulcer, swollen lymph nodes and butterfly-shaped red rash on the face, is a rare inflammatory rheumatic disease that attacks normal healthy tissues in the body. The major representation is lupus nephritis (LN) with severe kidney destruction. The study explains the relationship between the expression of inflammasome and LN. Tsai et al reported inhibiting the expression of mRNA and production of IL-1β, IL-18, caspase-1 relieves the symptom of LN. Ka et al further reported that a main active ingredient in the herbal medicine Litsea cubeca, significantly inhibited activation of NLRP3 inflammasome and caspase-1 and the secretion of IL-1. Moreover, it effectively ameliorated LN symptoms in accelerated and severe LN mice.
d. Interleukin and Crohn's Disease
Crohn’s disease (CD) is a chronic inflammatory condition of the GI tract with no known cure. It is demonstrated efficient to take antibody-based therapies directed against TNF or interleukin-12/interleukin-23 p40 subunit antibody or integrins in moderate-to-severe CD. However, many patients experience primary non-response or lose response over time to anti-TNF therapy, so that we require dose adjustment, or switch to a non-anti-TNF therapy. Interleukin-6 has multiple pro-inflammatory effects such as inhibition of apoptosis in T-cells and is a target for curing CD. A recent study of the IL-6 receptor inhibitor, tocilizumab, manifests a clinical benefit in moderate-to-severe CD.
Join the 25,000 subscribers to get research hotpots, technical tips, latest information on events, sales and offers.
Sign up now!
We don't deal in spam.