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Interleukin (IL) Family related Drugs

Glucocorticoids are chemicals that can suppress the cell-mediated immunity by stopping Inflammation. Inflammation is the source of many illnesses, for instance, autoimmune diseases and allergies. Glucocorticoids function by inhibiting the secretion of some cytokines, including Interleukin (IL) 1, IL 2, IL 3, IL 4, IL 5, IL 6, IL 8, and TNF. The decrease of cytokine production leads that T cell proliferation reduces. What’s more, glucocorticoids can suppress the humoral immunity which leads B cells to express fewer amounts of IL 2 and IL 2 receptors.

Ciclosporin is designed to suppress the immune system. Cyclosporine binds to the cytosolic protein cyclophilin which is an immunophilin in activated lymphocytes to form a complex. This complex inhibits the function of phosphatase calcineurin, which induces the transcription of interleukin-2. Ciclosporin also suppress interleukin release, leading to a reduced activated T cells.

Monoclonal antibodies can combine exactly defined antigens so that they cause fewer side-effects. The IL 2 receptor (CD25) and CD3-directed antibodies are used to reduce the rejection in transplanted organs. Interleukin-2 is a key regulator necessary for the clone expansion and survival of activated T cells. Researchers have tried to develop effective and safe anti-IL 2 antibodies. These drugs function by binding to the IL 2a receptor and prevent IL 2. Thus, the IL 2 induced clonal expansion of activated lymphocytes is reduced. A TNFα binding protein is also a monoclonal antibody which can bind to TNFα, preventing TNFα inducing the secretion of IL 1 and IL 6 and the adhesion of lymphocyte-activating molecules.

Related literatures

1. Gillett N A, Chan C. Applications of immunohistochemistry in the evaluation of immunosuppressive agents[J]. Human & experimental toxicology, 2000, 19(4): 251-254.

2. Olsson I, Gatanaga T, Gullberg U, et al. Tumour necrosis factor (TNF) binding proteins (soluble TNF receptor forms) with possible roles in inflammation and malignancy[J]. European cytokine network, 1992, 4(3): 169-180.

3. Borel J F, Feurer C, Magnee C, et al. Effects of the new anti-lymphocytic peptide cyclosporin A in animals[J]. Immunology, 1977, 32(6): 1017.

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