Regulation of Toll-like Receptor Signaling by the SF3a mRNA Splicing Complex


Within minutes after we are exposed to pathogens, our bodies react with a rapid response known as the “innate immune response.” This arm of the immune response regulates the process of inflammation, in which various immune cells are recruited to sites of infection and are activated to produce a host of antimicrobial compounds. This response is critical to fight infection. However, this response, if it is activated too strongly or if it becomes chronic, can do damage and can contribute to numerous very common diseases ranging from atherosclerosis to asthma to cancer. Thus it is essential that this response be tightly regulated, turned on when we have an infection, and turned off when not needed. We are investigating a mechanism that helps turn off this response, to ensure that inflammation is limited to prevent inflammatory disease. This mechanism involves the production of alternate forms of RNAs and proteins that control inflammation. We have discovered that a protein known as SF3a1 can regulate the expression of these alternate inhibitory RNA forms and are investigating how to use this knowledge to better control inflammation.


Vyšlo v časopise: Regulation of Toll-like Receptor Signaling by the SF3a mRNA Splicing Complex. PLoS Genet 11(2): e32767. doi:10.1371/journal.pgen.1004932
Kategorie: Research Article
prolekare.web.journal.doi_sk: 10.1371/journal.pgen.1004932

Souhrn

Within minutes after we are exposed to pathogens, our bodies react with a rapid response known as the “innate immune response.” This arm of the immune response regulates the process of inflammation, in which various immune cells are recruited to sites of infection and are activated to produce a host of antimicrobial compounds. This response is critical to fight infection. However, this response, if it is activated too strongly or if it becomes chronic, can do damage and can contribute to numerous very common diseases ranging from atherosclerosis to asthma to cancer. Thus it is essential that this response be tightly regulated, turned on when we have an infection, and turned off when not needed. We are investigating a mechanism that helps turn off this response, to ensure that inflammation is limited to prevent inflammatory disease. This mechanism involves the production of alternate forms of RNAs and proteins that control inflammation. We have discovered that a protein known as SF3a1 can regulate the expression of these alternate inhibitory RNA forms and are investigating how to use this knowledge to better control inflammation.


Zdroje

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