MAPK is also involved in T production and cell activation of cytokines, including IL 10 and also modulates IL 4 mediated reactions in T cells by cross talk with STAT6. This illustrates the multiple roles of this signaling pathway and how modulation of its activity might have multiple effects both on innate and adaptive mGluR immunity. Other signaling pathways that have been proved to be stimulated and involved in regulation of gene expression throughout inflammation and immune response such as Notch, Wnt and PI3 kinase pathways take part in host microbe relationships, but have not been studied in the context of periodontal illness. Because the cytokine network founded in diseased periodontal tissues is very complex and may be subject to shifts depending on infection activity, and also due to the repetitive and overlapping role of several cytokines, knowing the signaling pathways involved in cytokine gene expression may give and alternative approach Ivacaftor molecular weight for the modulation of host response affecting the whole cytokine profile. Cells of the immune system keep rigid control within the production of potentially dangerous cytokines by repressing their expression at the post transcriptional level. The adenine and uridine rich elements, located in the 3 untranslated region of many cytokines and other proinflammatory elements, plays a major part in post transcriptional repression. The clear presence of an ARE in a specific log can target it for rapid degradation or prevent translation. MRNA stability is dictated by inflammatory stimuli through signaling mechanisms. In the presence of inflammatory stimuli, AREs from 3 UTRs of IL 6, Infectious causes of cancer IL 8, COX 2, and TNF mediate regulation of mRNA stability by p38 MAPK. p38 MAPK is phosphorylated and activated by upstream kinases MKK3 and MKK6 when stimulated by IL 1B, TNF or LPS. p38 MAPK then phosphorylates MK2 which phosphorylates RNA binding proteins to manage mRNA stability. As it could affect the expression of numerous cytokines, producing a more extensive and complete change in the cytokine network established by the host response to the microbial aggression adjustment of signaling pathways is possibly quite promising for therapeutic applications in periodontal diseases. Taking into consideration the connection reversible 5-HT receptor agonist and antagonist of p38 MAPK pathway with signaling of tension and inflammatory/infectious stimuli, we have dedicated to studying the potential of modulating this pathway to affect the appearance of some pro inflammatory cytokines which can be especially appropriate for host mediated destruction of mineralized and nonmineralized tissues in periodontal disease. In vitro evidence for the meaning of p38 MAPK to periodontal disease is generally produced from studies showing the important role of this signaling pathway to the regulation of expression of inflammatory cytokines that are relevant to the disease process.