TLR regulation of pro-inflammatory cytokines. Activation of toll-like receptors and type I IL-1 receptors evoke inflammation in immune cells by sharing signaling cascades. TLRs expressed on professional immune cells (macrophages, dendritic, monocytes and microglia cells) discern and respond to helminth infection. TLRs are triggered by helminth or helminth products containing pathogen-associated molecular patterns (PAMPs). All TLR family members and the type I interleukin-1 receptor (IL-1RI) have specific intracellular TIR signaling domains. In response to activation by the corresponding ligands, TIR domains react with the TIR domains of the signaling adaptor MyD88, which convey the signal to a family of IL-1 receptor-associated kinases (IRAKs). Phosphorylation of IRAK, a serine-threonine kinase, by other IRAK family members provoke cascades of signaling through tumor necrosis factor receptor-associated factor 6 (TRAF6). TRAF6 relays a signal to I kappa B kinase (IKK) and to mitogen-activated protein kinase kinase (MAP3K). This signaling leads to transcriptional responses, mediated primarily by ERK, NF-κB and stress-activated protein kinases, for example JNK and p38, result in the expression of pro-inflammatory cytokines.