Putative inactive protein kinase which regulates signaling downstream of immune receptors including IL1R and Toll-like receptors (PubMed:12150927, PubMed:12054681, PubMed:29686383). Inhibits dissociation of IRAK1 and IRAK4 from the Toll-like receptor signaling complex by either inhibiting the phosphorylation of IRAK1 and IRAK4 or stabilizing the receptor complex (PubMed:12150927, PubMed:12054681). Upon IL33-induced lung inflammation, positively regulates expression of IL6, CSF3, CXCL2 and CCL5 mRNAs in dendritic cells (PubMed:29686383). Monomer (By similarity). Homodimer (By similarity). May interact with IRAK4 (when phosphorylated) (By similarity). Interacts (when phosphorylated at Thr-110) with PIN1 (via WW domain) in response to IL33-mediated (but not TLR4 ligand LPS) dendritic cell stimulation (PubMed:29686383). In dendritic cells, translocates into the nucleus upon IL33 stimulation. Expressed in inflamed lung macrophages (at protein level) (PubMed:29686383). Expressed in dendritic cells (at protein level) (PubMed:29686383). Highly expressed in liver and thymus and at lower levels in heart, brain, spleen and kidney (PubMed:12054681). The nucleotide binding domain binds ATP with low affinity. In response to intranasal administration of IL33, lung inflammation is reduced compared to wild-type and is associated with low infiltration by inflammatory cells, especially granulocytes, a severe reduction in Th2-type cytokine secretion, including Il4, Il5 and Il13 in bronchial alveolar fluids, and reduced up-regulation of Il6, Csf3, Cxcl2 and Ccl5 mRNAs. Belongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family. Pelle subfamily. Asn-306 is present instead of the conserved Asp which is expected to be an active site residue. Low level autophosphorylation activity has been reported in PubMed:12054681, while other authors describe this as an inactive kinase.