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This 2 page Class Notes was uploaded by Jacob Decker on Saturday February 13, 2016. The Class Notes belongs to ZOL 425 at Michigan State University taught by D. Bello-Deocampo in Spring 2016. Since its upload, it has received 25 views. For similar materials see Cells and Development (W) in Microbiology at Michigan State University.
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Date Created: 02/13/16
Decker 1 William Decker ZOL 425 1/26/16 Homework 2: Summary of “Inflammation in prostate carcinogenesis” Recently, great attention has been drawn to the subject of immunity and the role of toll like receptors (TLRs). Latest research has acknowledged the importance of TLRs in “recognizing specific microbial components derived from pathogens including bacteria, fungi, 1 protozoa and viruses” which, in effect, causes a proliferation of effector molecules, chemokines and assorted proinflammatory cytokines. Ten classes of TLR ligands are located in the membranes of macrophages and dendritic cells, whose role is the phagocytosis and endocytosis of pathogenic substances. TLRs also upregulate the expression of major histocompatibility 2 complex II (MHC II) molecules. MHC II molecules are then used by macrophages and dendritic cells which facilitate responses from the adaptive immune system. Along with the adaptive immune system, TLRs also have a significant function in inflammatory responses. The recognition of pathogens by TLRs promotes their own self dimerization, which then results in the activation of signaling pathways from the cytoplasmic 3 TIR (TollInterleukin) domain. Although signaling pathways of TLRs are divergent, a subsequential TIRdomain adaptor called MyD88 is mutually involved with all TLRs. MyD88 produces cytokines such as TNF and IL12, which are critical in the body’s inflammatory response. Inflammation is a protective response of the body to ridden the source of the cellular damage and mediate reparation. Inflammation can be harmful to the body if not administered in _____________________________________________________ 1 Kiyoshi Takeda and Shizuo Akira. “Tolllike receptors in innate immunity.” International Immunology, Vol. 17, No. 1, 2005): 2. 2 Angelo M. De Marzo et al. “Inflammation in prostate carcinogenesis.” Nature Reviews Cancer (2007): 264. 3 Takeda and Akira. “Tolllike receptors,” 5. 4 5 Takeda and Akira. “Tolllike receptors,” 6. Takeda and Akira. “Tolllike receptors,” 8. Decker 2 the right doses. Too little could allow the source (pathogen) to continue cellular damage, but excess cytokine production brings a high mortality rate from serious systemic disorders. 5 To prevent this overproduction of cytokines, there are molecules responsible for the negative regulation of TLR signaling. Single immunoglobulin IL1 receptorrelated molecule (SIGIRR) and T1/ST2, for example, are membrane proteins that when absent or deficient cause 6 an increased inflammatory response in the body. There are, however, times when down regulation fails and a serious and lifethreatening chronic inflammatory state is established. In fact, a study took place in Sweden that implied strong correlations of chronic inflammation and the development of cancer. Carriers of a single nucleotide polymorphism in TLR4 had a 26% morelikely chance of prostate cancer and were 39% more at risk of earlyonset prostate cancer compared with those without this genetic mutation. It is safe to assume, then, that because this lineage of genes is so closely related to adaptive immunity, errors in the mechanisms of inflammation are significant in the advancement of cancer. _____________________________________________________ 6Takeda and Akira. “Tolllike receptors,” 8. 7 De Marzo. “Inflammation in prostate carcinogenesis,” 256. 8 De Marzo. “Inflammation in prostate carcinogenesis,” 264.
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