Interleukin 16, also known as lymphocyte chemoattractant factor (LCF), refers to the C-terminal peptide of Mouse pro-IL-16 or neuronal IL-16, which are nuclear and cytoplasmic PD2 domain containing proteins. The C-termini of these proteins are cleaved by Caspase-3, resulting in the release of secreted IL-16. Mature IL-16 has been shown to bind the cell surface receptor CD4 and function as an immunomodulatory cytokine. The C-terminal peptide of human and Mouse IL-16 share approximately 86% amino acid sequence identity.
IL17, also known as IL17a, is a cytokine that belongs to the IL-17 family. Cytokines are proteinaceous signaling compounds that are major mediators of the immune response. They control many different cellular functions including proliferation, differentiation, and cell survival/apoptosis but are also involved in several pathophysiological processes including viral infections and autoimmune diseases. Cytokines are synthesized under various stimuli by a variety of cells of both the innate(monocytes, macrophages, dendritic cells) and adaptive(T- and B-cells) immune systems. The IL-17 family of cytokines includes six members, IL-17/IL-17A, IL-17B, IL-17C, IL-17D, IL-17E/IL-25, and IL-17F, which are produced by multiple cell types. IL-17 regulates the activities of NF-kappaB and mitogen-activated protein kinases. This cytokine can stimulate the expression of IL6 and cyclooxygenase-2(PTGS2/COX-2), as well as enhance the production of nitric oxide(NO) . High levels of IL-17 are associated with several chronic inflammatory diseases including rheumatoid arthritis, psoriasis, and multiple sclerosis.
Interleukin-17 is a potent pro-inflammatory cytokine produced by activated memory T cells. There are at least six members of the IL-17 family in humans and in mice. Mature mouse IL-17A shares 61% and 89% amino acid sequence identity with human and rat IL-17A, respectively. As IL-17 shares properties with IL-1 and TNF-alpha, it may induce joint inflammation and bone and cartilage destruction. This cytokine is found in synovial fluids of patients with rheumatoid arthritis, and produced by rheumatoid arthritis synovium. It increases IL-6 production, induces collagen degradation and decreases collagen synthesis by synovium and cartilage and proteoglycan synthesis in cartilage. IL-17 is also able to increase bone destruction and reduce its formation. Blocking of interleukin-17 with specific inhibitors provides a protective inhibition of cartilage and bone degradation.
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