◀ Back to IL15

IL15 — MYD88

Text-mined interactions from Literome

Oshikawa et al., Biochem Biophys Res Commun 2003 (Lung Diseases) : The results demonstrated three patterns of gene expression : the TLR2 and myeloid differentiation factor 88 ( MyD88 ) gene expressions were induced in AM in response to lipopolysaccharide (LPS), interleukin (IL)-1beta , or tumor necrosis factor-alpha or in the lung tissue of an LPS induced acute lung injury model ; the gene expressions of TLR1, -3, -6, CD14, and MD2 were unchanged ; and the TLR4 and TLR5 gene expressions were downregulated in AM following inflammatory stimuli
Yu et al., J Immunol 2006 (Lymphopenia) : These results suggest that parenchymal cells such as i-ECs contribute to the maintenance of CD8alphaalpha TCRalphabeta and gammadelta i-IELs at least partly via MyD88 dependent IL-15 production
Rad et al., Gastroenterology 2007 (Gastritis...) : The adaptor protein Myd88 mediates Toll-like receptor ( TLR ), interleukin (IL)-1 , and IL-18 signaling
Leichtle et al., BMC immunology 2009 (Otitis Media) : Activated TLRs signal via two alternative intracellular signaling molecules with differing effects ; MyD88 ( Myeloid differentiation primary response gene 88 ) inducing primarily interleukin expression and TRIF ( Tir-domain containing adaptor inducing interferon beta ) mediating type I interferon ( IFN ) expression
Kissner et al., Innate Immun 2011 (Disease Models, Animal...) : Our results indicated that elevated tumor necrosis factor-a, interferon-?, interleukin (IL)-1a/ß and IL-6 production from mouse spleen cells treated with SEB alone or in combination with lipopolysaccharide (LPS) was regulated by MyD88
Colpitts et al., J Immunol 2012 (Vesicular Stomatitis) : Cutting edge : the role of IFN-a receptor and MyD88 signaling in induction of IL-15 expression in vivo