The history of interleukin-6 (IL-6) dates back to the late 1960s when it was hypothesized that a T cell-derived soluble factor would be involved in B cell activation, which was initially named B cell stimulatory factor-2 (BSF-2). In 1986 the complementary DNA encoding this factor was cloned and the name IL-6 was introduced.
Figure This is a crystal structure of human IL-6 created using the data from Protein Data Bank (PDB: 1ALU) and rendered using PyMOL.
Interleukin-10 (IL-10), also known as human cytokine synthesis inhibitory factor (CSIF), is a cytokine encoded by the IL-10 gene in humans, located on chromosome 1. The protein has a length of 178 amino acids and functions as a homodimer.
Figure The figure on the right side shows a structure of IL-10 created using the data from Protein Data Bank (PDB: 2H24) and rendered using PyMOL.
U-CyTech biosciences offers a wide variety of high-quality colorimetric-based ELISA kits for the measurement of cytokines, chemokines and granzymes from different species (human, monkey, mouse and rat). Currently, U-CyTech's product range has been expanded with 3 specific ELISA kits for the detection of human IL-7, human IP-10 and monkey IP-10.
Human IL-13 is a 17-kDa glycoprotein primarily produced by activated Th2 cells. IL-13 is involved in several stages of B-cell maturation and differentiation. It up-regulates CD23 and MHC class II expression, and promotes IgE isotype switching of B cells. Other activities include down-regulation of macrophage activity and inhibition of the production of pro-inflammatory cytokines and chemokines. The IL-13 gene is located on chromosome 5q31 and forms a cytokine gene cluster with IL-3, IL-5, IL-4, and GM-CSF, with IL-13 remarkably close to IL-4. The IL-13 and IL-4 genes exhibit a 30% sequence homology, have a similar structure and the same orientation suggesting that these genes arose as a duplication event during evolution.
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Cancer immunology, immunotherapy : CII
2010 Feb;59: 279-91
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Till now, little is known about the effects of chemotherapy on the immunity of cancer patients and the ideal timing ("window" period) for immunotherapy combined with chemotherapy. In this study, we addressed the immunogenicity of apoptotic ovarian cancer cells induced by paclitaxel and carboplatin, the immunologic aspects in ovarian cancer patients under chemotherapy, and the CTL response when CD8(+) T cells were stimulated with tumor antigen in the "window" period. The immunogenicity of apoptotic ovarian cancer cells was detected first.