Most metazoan mitochondrial genomes are circular, have a length of approximately 16 kb and encode 37 genes including 13 proteincoding genes, two rRNA genes, and 22 tRNA genes. The databases presently include the mitochondrial genomes of 37 acarids, including 12 of the superorder Acariformes and 25 of the superorder Parasitiformes. Several aspects of the mt-genomes of Acari have been examined, including gene rearrangement, tRNA gene loss and atypical short tRNA. Sequencing these genomes will have other benefits. For example it should provide insights into the molecular evolution of acaricideresistance genes. The rapid development of acaricide resistance of spider mites is a long-standing problem. Several acaricides have been identified as mitochondrial respiration inhibitors. Resistance to the acaricide bifenazate has been correlated with mutations in the mitochondrial cytochrome b gene. The genomes will also provide information on gene rearrangements, evolutionary pattern and structure of the control region, strand asymmetry in nucleotide composition and RNA secondary structure. Monocytes are circulating mononuclear phagocytes that have been generally regarded as systemic precursors for tissue macrophages and inflammatory dendritic cells. Besides their primary role as a precursor, monocytes function as important innate effectors against pathogens through phagocytosis, production of reactive oxygen species, and secretion of proinflammatory cytokines. It is clear that monocytes are also involved in the pathogenesis of many chronic inflammatory diseases such as RA, Crohn’s diseases, and atherosclerosis. RA is a systemic and chronic autoimmune disease that primarily targets synovial membranes. Despite extensive studies, the cause of RA is still unknown although a complex interplay among genetic factors and environmental triggers are thought to be involved. The presence of autoantibodies Foretinib generated via Tcell-dependent processes in RA patients and mouse models underscore the importance of adaptive immunity as the central contributor to early pathogenesis ; however, a growing body of evidence has revealed that a variety innate effector cells, such as monocytes/macrophage, are also closely involved in the development of synovial inflammation in RA. Co-signaling molecule networks among immune cells are critical for controlling the immune response. Among these, the B7 superfamily is major co-signaling molecules acting as a checkpoint in the modulation of T-cell responses. Given that in vivo activated-monocytes derived from synovial fluid of active RA patients promote pathogenic Th17 responses through cell contact, it was suggested that differential expression of co-signaling molecules might be responsible.