People with rheumatoid arthritis often receive medications that target and inhibit Tumor-Necrosis Factor (TNF), a protein involved in the painful and damaging inflammation characteristic of the disease. While several anti-TNF drugs are used widely with comparable clinical success, the details of their different molecular effects on biological processes have been unclear.
To fill this gap, Karagianni and colleagues employed a mouse model of chronic inflammatory polyarthritis -- mice that express the human TNF and develop symptoms and signatures that closely mirror the human form of the disease. The diseased mice received treatment with one of four anti-TNF drugs (Remicade, Cimzia, Humira, or Enbrel), or for comparison, none of the drugs. The researchers then compared them to healthy mice.
Treatment - Researchers - Tissue - Mice - Transcriptomes
After treatment, the researchers collected joint tissue from all the mice and analyzed their transcriptomes -- the complete set of messenger RNA molecules in the tissues, which indicates which genes are turned on or off. Then, they applied...
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